United States
Environmental Protection
Agency
Office of Water August 1982
Regulations and Standards (WH-553) EPA-440/4-85-010
Washington DC 20460
Water
An Exposure
and Risk Assessment
for Lead
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DISCLAIMER
This is a contractor's final report, which has been reviewed by the Monitoring and Data Support
Division, U.S. EPA. The contents do not 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.
U.S. Environmental Protection Agency
Region 5, Library (PH2J)
77 West Jackson Boulevard, 12th Ftaw
CWc«$o, IL 60504.3590
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50J72-10t
REPORT DOCUMENTATION *• «EPORT NO. 2.
PAGE EPA-440/4-85-010
4. Titla and Subtitle
An Exposure and Risk Assessment for Lead
7. Authoru) Perwak, J.; Goyer, M. ; Nelken, L.;
Payne, E.; and Wallace, D.
9. Performing Organization Nama and Address
Arthur D. Little, Inc.
20 Acorn Park
Cambridge, MA 02140
12. Sponsoring Organization Nama and Address
Monitoring and Data Support Division
Office of Water Regulations and Standards
U.S. Environmental Protection Agency
Washington, D.C. 20460
3. Recipient's Accacaion No.
s. Report Data Final Revision
Aueust 1982
6.
8. Parforming Organization Rapt. No.
10. Projact/Taak/Work Unit No.
11. Contract(C) or Grant(G) No.
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EPA-440/4-85-010
July 1981
(Revised August 1982)
AN EXPOSURE AND RISK ASSESSMENT
FOR LEAD
DV
Joanne Perwal;
Muriel Goyer, Leslie Nelken,
Edmund Payne, Douglas Wallace
Arthur D. Little, Inc.
U.S. EPA Contract 68-01-5949
Richard Healy
Project Manager
U.S. Environmental Protection Agency
Monitoring and Data Support Division (WH-553)
Office of Water Regulations and Standards
Washington, D.C. 20460
OFFICE OF WATER REGULATIONS AND STANDARDS
OFFICE OF WATER AND WASTE MANAGEMENT
U.S. ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20460
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FOREWORD
Effective regulatory action for toxic chemicals requires an
understanding of the human and environmental risks associated with the
manufacture, use, and disposal of the chemical. Assessment of risk
requires a scientific judgment about the probability of harm to the
environment resulting from known or potential environmental concentra-
tions. The risk assessment process integrates health effects data
(e.g., carcinogenicity, teratogenicity) with information on exposure.
The components of exposure include an evaluation of the sources of the
chemical, exposure pathways, ambient levels, and an identification of
exposed populations including humans and aquatic life.
This assessment was performed as part of a program to determine
the environmental risks associated with current use and disposal
patterns for 65 chemicals and classes of chemicals (expanded to 129
"priority pollutants") named in the 1977 Clean Water Act. It includes
an assessment of risk for humans and aquatic life and is intended to
serve as a technical basis for developing the most appropriate and
effective strategy for mitigating these risks.
This document is a contractors' final report. T.t has been
extensively reviewed by the individual contractors «?nd by the EPA at
several stages of completion. Each chapter of the draft was reviewed
by members of the authoring contractor's senior technical staff (e.g.,
toxicologists, environmental scientists) who had not previously been
directly involved in the work. These individuals were selected by
management to be the technical peers of the chapter authors. The
chapters were comprehensively checked for uniformity in quality and
content by the contractor's editorial team, which also was responsible
for the production of the final report. The contractor's senior
project management subsequently reviewed the final report in its
entirety.
At EPA a senior staff member was responsible for guiding the
contractors, reviewing the manuscripts, and soliciting comments, where
appropriate, from related programs within EPA (e.g., Office of Toxic
Substances, Research and Development, Air Programs, Solid and
Hazardous Waste, etc.). A complete draft was summarized by the
assigned EPA staff member and reviewed for technical and policy
implications with the Office Director (formerly the Deputy Assistant
Administrator) of Water Regulations and Standards. Subsequent revi-
sions were included in the final report.
Michael W. Slimak, Chief
Exposure Assessment Section
Monitoring & Data Support Division (WH-553)
Office of Water Regulations and Standards
iii
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TABLE OF CONTENTS
Page
LIST OF TABLES ix
LIST OF FIGURES
XI
1.0 TECHNICAL SUMMARY 1_1
1.1 Risk Considerations 11
1.1.1 Humans 1 •,
1.1.2 Biota £3
1.2 Sources of Lead to the Environment j__4
1.3 Fate and Distribution of Lead in the Environment 1-5
2.0 INTRODUCTION 2-i
3.0 MATERIALS BALANCE 3_1
3.1 Introduction 3 ,
3.2 Production of Lead 3 /
3.2.1 Primary Production 3_4
3.2.2 Secondary Production 3_7
3.3 Uses of Lead 2_g
3.3.1 Emissions from the Use of Lead 3-11
3.3.2 Inadvertent Sources of Lead Emissions 3-H
3.4 Future Projections for Lead 3_12
3.5 Summary 3-12
4.0 FATE AND DISTRIBUTION OF LEAD IN THE ENVIRONMENT 4-1
4.1 Introduction ,_,
4.2 Distribution of Lead in the Environment 4_1
4.2.1 Water and Sediment ^
4.2.1.1 Freshwater 4_-L
4.2.1.2 Seawater 4-1
4.2.1.3 Rainfall 4_4
4.2.1.4 Urban Runoff 4_4
4.2.1.5 STORET Data 4_4
4.2.1.6 Lead in Sediment /. e.
4.2.2 Air , °
4.2.3 Soil I
4.2.4 Biota £-13
4.2.5 Limitations of Monitoring Data 4_13
4.3 Fate of Lead in the Environment 4-15
4.3.1 Introduction -
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TABLE OF CONTENTS (Continued)
4.3.2 General Fate Processes
4.3.2.1 Atmospheric Transport
4.3.2.2 Fate Processes in Aquatic Environments
4.3.2.3 Fate Processes in Terrestrial Environments
4.3.3 Major Environmental Pathways
4.3.3.1 Pathway ?fl — Atmospheric Transport
4.3.3.2 Pathway #2 -- Solid Wastes, Tailings,
and Municipal Landfills
4.3.3.3 Pathway #3 — Aqueous Industrial Discharge
4.3.3.4 Pathway #4 — Publicly-owned Treatment Works
4.4 Overview
4.4.1 Atmospheric Levels and Pathways
4.4. 2 Aquatic Levels and Pathways
4.4.3 Terrestrial Levels and Pathwavs
5.0 HUMAN EFFECTS AND EXPOSURE
5-1
5.1 Human Toxicity 5_]_
5.1.1 Introduction 5_1
5.1.2 Metabolism and Bioaccumulation 5-1
5.1.2.1 Absorption 5-1
5.1.2.2 Distribution and Retention 5-3
5.1.2.3 Elimination 5-4
5.1.2.4 Metabolism of Organolead Compounds 5-4
5.1.3 Human and Animal Studies 5-4
5.1.3.1 Carcinogenesis 5-5
5.1.3.2 Mutagenesis 5-7
5.1.3.3 Adverse Reproductive Effects 5-8
5.1.3.4 Other Toxic Effects 5-11
5.1.4 Overview 5-16
5.1.4.1 Ambient Water Quality Criteria - Human Health 5-16
5.1.4.2 Other Considerations 5-17
5.2 Human Exposure 5-19
5.2.1 Introduction 5-19
5.2.2 Populations Exposed Through Food 5-20
5.2.2.1 Pathways of Exposure 5-20
5.2.2.2 Total Dietary Intake — Adults 5-24
5.2.2.3 Total Dietary Intake — Infants and Children 5-24
5.2.3 Populations Exposed Through Drinking Water 5-25
5.2.3.1 Pathways of Exposure 5-25
5.2.3.2 Drinking Water Exposure — Adults 5-26
5.2.3.3 Drinking Water Exposure — Infants and
Children 5-26
5.2.4 Populations Exposed Through Inhalation (Air, Dirt,
and Dust) ' 5_26
5.2.4.1 Pathways of Exposure 5-26
vi
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TABLE OF CONTENTS (Continued)
5.2.4.2 Inhalation Exposure — Adults 5-28
5.2.4.3 Inhalation Exposure — Infants and Children 5-28
5.2.5 Populations Exposed Through Other Routes 5-28
5.2.5.1 Cigarettes 5-28
5.2.5.2 Dirt and Dust 5-28
5.2.5.3 Paint 5-29
5.2.5.4 Other Routes 5-29
5.2.6 Blood Levels Associated with Various Subpopulations 5-29
5.2.7 Summary — Exposure Scenarios 5-33
5.2.7.1 Introduction 5-33
5.2.7.2 Exposure Estimates 5-33
6.0 BIOTIC EFFECTS AND EXPOSURE . 6-1
6.1 Effects on Biota 6-1
6.1.1 Introduction 6-1
6.1.2 Freshwater Organisms 6-1
6.1.2.1 Chronic and Sublethal Effects 6-1
6.1.2.2 Acute Toxicity 6-3
6.1.2.3 Effects on Microflora 6-3
6.1.3 Marine Organisms 6-6
6.1.4 Factors Affecting the Aquatic Toxicity of Lead 6-6
6.1.5 Terrestrial Organisms 6-9
6.1.5.1 Animals 6-9
6.1.5.2 Plants 6-10
6.1.6 Summary 6-11
6.2 Exposure to Biota 6-13
6.2.1 Introduction 6-13
6.2.2 Aquatic Organisms 6-14
6.2.2.1 Pathways of Exposure
6.2.2.2 Environmental Factors Affecting Lead
Exposure and Uptake 6-15
6.2.2.3 Monitoring Data 6-16
6.2.3 Terrestrial Organisms 6-16
6.2.3.1 Mammals 6-16
6.2.3.2 Birds 6-18
6.2.3.3 Terrestrial Plants 6-20
6.2.3.4 Summary 6-21
7.0 RISK CONSIDERATIONS 7-1
7.1 Humans 7-1
7.1.1 Introduction 7-1
7.1.2 Adults 7-4
7.1.3 Children 7-6
vii
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TABLE OF CONTENTS (Continued)
Page
7.2 Risks to Biota 7.5
7.2.1 Aquatic Organisms 7_6
7.2.2 Terrestrial Organisms 7-10
7.2.2.1 Mammals 7-10
7.2.2.2 Birds 7_10
7.2.2.3 Plants 7_H
APPENDIX A NOTES ON THE DERIVATION OF TABLE 3-1 A-l
viii
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LIST OF TABLES
Table
No.
Page
3-1 Summary of U.S. Supply, Use, and Emissions, 1976 3-2
3-2 Capacities and Locations of U.S. Lead Smelters
and Refineries, 1977 3.5
3-3 U.S. Leading Lead-Producing Mines in Order of
Output, 1975 3_6
3-4 U.S. Supply and Demand Relationships of Lead, 1965-76 3-10
3-5 U.S. Forecasts for Lead Demand, 1976 and 2000 3-13
3-6 Summary of World Lead Reserves 3_14
4-1 Concentrations of Lead in Water 4-2
4-2 Concentrations of Lead in Sediment 4-3
4-3 Mean and Maximum Ranges of Lead Concentrations 4-7
4-4 Concentrations of Lead in the Atmosphere 4-9
4-5 Concentrations of Lead in the Soil 4_H
4-6 Concentrations of Lead in Biota 4-14
4-7 Concentration and Distribution of Lead in the
Water Column 4-22
4-8 Lead Bioaccumulation Levels and Bioconcentration
Factors in Aquatic Species 4-24
4-9 Lead Accumulation by Vegetation 4-31
4-10 Effluent Data From U.S. Municipal Treatment Plants
Using Various Treatment Methods 4-44
5-1 Human Exposure to Lead Through Inhalation 5-27
5-2 Exposure Estimates of Lead for Adults and Children
Living in Rural, Urban, and Industrial Environments 5-34,35,36
6-1 Sublethal Effects of Lead on Freshwater
Fish 6_2
6-2 Chronic and Sublethal Effects of Lead on
Freshwater Invertebrates 6_4
ix
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LIST OF TABLES (Continued)
Table
No- Page
6-3 Acute Toxicity (LC5Q) of Lead to Freshwater Fauna 6-5
6-4 Acute Toxicity (LC5Q) of Lead to Marine Invertebrates 6-7
6-5 Measurements of Total Lead Concentrations in or
U.S. Minor River Basins, 1979 6_17
7-1 Adverse Effects of Lead on Humans 7-2
7-2 Human Exposure to Lead as Evidenced by Blood
Levels in the United States 7-5
7-3 Concentrations of Lead in Water 7-9
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LIST OF FIGURES
Figure
No.
3-1 Environmental Flow of Lead, 1976 (kkg) 3.3
4-1 Mean Ambient Values of Lead Concentrations in
U.S. Surface Waters, 1970-79 (Detected Levels Only) 4-5
4-2 Major Environmental Pathways of Lead Emissions 4-16,17
4-3 Schematic Diagram of Major Pathways of
Anthropogenic Sources of Lead Released to the
Environment in the United States, 1976 4_13
4-4 Adsorption of Heavy Metals in Oxidizing Fresh Waters 4-21
4-5 Adsorption of Heavy Metals on Soil Minerals and Oxides 4-27
4-6 Downward Movement of Lead in Soil 4_2s
5-1 Population Exposure Routes for Lead 5_2i
5-2 Exposure Scenarios — Adults (Absorbed Dose) 5-37
5-3 Exposure Scenarios — Children with Pica (Absorbed Dose) 5-38
xi
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ACKNOWLEDGMENTS
The Arthur D. Little, Inc., Task Manager for this report was Joanne
Perwak. Other major contributors were Melba Wood and Edmund Payne
(monitoring data), Leslie Nelken (environmental fate), Muriel Cover
(human effects and risk), and Douglas Wallace (aquatic effects and
exposure). Alfred Wechsler and Kate Scow reviewed this document. In
addition, Laura Williams, Nina Green, and Irene Rickabaugh were respon-
sible for editing and report production.
The materials balance for lead (Chapter 3.0) was provided by
Versar, Inc. Gay Contos was the Task Manager for Versar.
Richard Healy, Richard Silver, and Ruth Wilbur reviewed the document
at U.S. EPA.
Kill
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1.0 TECHNICAL SUMMARY
The Monitoring and Data Support Division, Office of Water Regulations
and Standards of the U.S. Environmental Protection Agency is conducting
risk assessments for pollutants that may enter and traverse the environ-
ment, thereby leading to exposure to humans and other biota. The program
is in response to Paragraph 12 of the NRDC Consent Decree. This report is
a risk assessment for lead using available data and quantitative models
where possible to evaluate overall risk.
1.1 RISK CONSIDERATIONS
Children are particularly susceptible to the toxic effects of lead
and lead exposure is still considered a major problem for children in the
United States today. Lethalities are not as common as they once were;
however, long-term effects such as learning and behavioral'problems may
occur, and remain after symptoms of clinical lead toxicity have disappeared.
Ingestion of paint chips is considered the major source of lead exposure in
children, especially in those from 1-3 years of age. Ingestion of contami-
nated dirt and dust is also a significant source of exposure in the vicinity
of heavy traffic areas and industrial areas, especially smelters.
In adults, the effects of lead toxicity are on a much more limited
scale. The primary exposure route is through food; a large part of this
exposure results from processing and contamination of canned goods with
lead solder. In isolated situations of high concentration of lead in air
or drinking water, however, these pathways can dominate food exposure. Lead
poisoning has also been observed in adults as a result of moonshine consump-
tion, and the consumption of food from improperly glazed earthenware.
Risk to aquatic organisms as a result of exposure to lead does not
appear to be widespread, because lead concentrations in the aquatic envi-
ronment are generally low compared to levels at which effects are generally
observed. Waterfowl, however, are still at risk because of exposure to
lead shot. The use of lead shot, however, is being severely limited, and
this problem is expected to diminish rapidly.
1.1.1 Humans
The effects of lead on humans have been extensively studied. However,
exposure levels that were once considered acceptable have been lowered
because of the increasing evidence of subtle effects at blood lead values
that result in no overt symptoms of lead toxicosis.
Although human data on the carcinogenicity of lead are limited, no
evidence suggests that lead is carcinogenic in humans. Feeding experi-
ments with rodents have indicated some carcinogenic activity; however,
this activity occurs at levels that are far in excess of the maximum
tolerated dose of lead in humans (550 mg elemental lead per day).
1-1
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Evidence for chromosomal abnormalities in humans resulting from
lead exposure is inconclusive and contradictory. Studies in animals
are also conflicting. However, lead can exert a profound, adverse
effect on the fetus and can interfere with the reproductive ability of
both men and women exposed to high levels (blood lead levels (PbB) of
30-40 ug/100 ml). Such levels are most common in occupational situa-
tions. Because the fetus develops so rapidly, it is particularly
vulnerable to intrauterine exposure to lead. Such effects as increased
incidences of stillbirths, preterm deliveries, and early fetal membrane
rupture have been associated with elevated exposure to lead. Incidences
of decreased fertility in occupationally-exposed men have also been
reported. However, no data suggest that lead is teratogenic in man.
Other toxic effects of lead are directed primarily at three target
organs; the erythroid cells of the bone marrow, the kidney, and the
central and peripheral nervous system. The inhibitory effects of lead
on erythropoiesis are reversible; however, severe acute or chronic lead
poisoning may be followed by irreversible injury to the kidney and
nervous system.
The disruption of hemoglobin synthesis is generally considered the
first observable adverse effect of lead exposure and is the effect most
commonly found. The inhibition of heme synthesis can eventually result
in clinical anemia at blood levels greater than 80 ug/100 ml in adults,
although mild anemia may occur at blood lead levels of 50 ug/100 ml.
Children may be affected at levels of about 40 ug lead/ml of blood.
A depression of ALAD (an enzyme necessary for the production of heme)
activity has been observed at PbB of 10-20 ug/100 ml or lower.
Proximal tubular dysfunction can occur in both children (PbB=40-120
Ug/100 ml) and adults (PbB >70 ug/100 ml) and is generally noted after
short-term exposure. Although little is known about dose-response
relationships, PbB greater than 70 ug/100 ml for prolonged periods may
give cause to irreversible functional and morphological renal changes.
The effects of lead on the central nervous system are probably the
most serious. Manifested as encephalopathy, effects on the central
nervous system are seen more frequently in children than adults. Com-
monly observed symptoms include dullness, hyperkinetic or aggressive
behavior, headaches, muscular tremors, hallucinations, and in severe
cases, convulsions, mania, paralysis, and coma. The minimal PbB levels
associated with encephalopathy are estimated to be about 30 ug/100 ml.
Subtle impairment of cerebral function has been observed at levels over
40 yg/100 ml. The peripheral nervous system may also be affected by
exposure to lead. Such effects as slowed nerve conduction have been
reported at blood levels exceeding 50 ug/100 ml.
The pathways of human exposure to lead are numerous and sometimes
complex. Food is generally considered the largest source of lead expo-
sure in adults, although both drinking water and air can be more
significant in some situations. Consumption of paint chips is considered
1-2
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an important source of lead in children, and probably the most widespread-
however, ingestion of dust and dirt may also be important in urban and
smelter areas. Sources of lead in the diet may include contamination
resulting from processing and lead-soldered cans, past use of lead arsen- •
ate pesticides, deposition on soil or plants from such sources as automo-
bile and smelter emissions, contamination of moonshine whiskey, leaching
from improperly glazed earthenware, and uptake from cooking water. The
contamination of food through the use of lead solder in cans represents
the most widespread source of lead in the diet. The "average" adult con-
sumes 100-200 yg lead/day in food, while children consume about 100 yg/day.
Up to 50% of this amount has been attributed to lead solder in cans.
Persons giving near sources of lead may consume more because of the con-
tamination of local crops.
Drinking water does not generally contribute greatly to human
exposure. However, concentrations greater than 50 tag/1 can result from
lead service lines, plumbing, solder, and storage containers.
Inhalation can be an important exposure pathway for adults in urban
or industrial areas (i.e. smelters). In these areas, the primary sources
of lead are automobiles and lead industries. The deposition of lead on
dirt and dust provides an important exposure route for children via
ingestion; however, this exposure route is not well quantified.
The ingestion of paint and contaminated soil is especially serious
in children having pica (tendency to ingest nonfood items). It has been
estimated that one-third to one-half of the 1-3-year-old children have
pica. However, little is known about their behavior or the amount
ingested.
An examination of the literature on human blood levels of lead
revealed a typical range of 9-24 yg/100 ml in the blood of adults. Most
of this (6-18 yg of lead per 100 ml of blood) is attributed to intake
from food. Assuming a log-normal distribution of blood levels, less than
5% of the urban population would have blood levels greater than 30 yg/100
ml, and less than 0.5% of the rural population. Mean levels greater than
20 yg/100 ml have been reported in adults in the immediate vicinity of
highways, and levels greater than 40 yg/100 ml in adults living near a
smelter.
_ Blood levels of lead in children are consistently higher than adults
in the same environment. Lead screening programs detect about 40,000
children annually with blood lead levels greater than 30 yg/100 ml.
Again, elevated blood levels (greater than 30-40 yg/100 ml) have been-
found in a large proportion of children living near roadways and urban
areas, in rural areas with lead paint problems, near primary and
secondary smelters, and near battery plants.
1.1.2 Biota
tal lrleitIUVff?CuS °f,lead in the laboratory (including developmen-
tal irregularities) have been observed at concentrations of less than
1-3
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10 ug/1 for rainbow trout in soft water. Several other freshwater fish
species are similarly affected in the range of 10-100 u*/l. 4 variety
or freshwater fish and invertebrate experience chronic toxic:tv in '
concentrations of 100-1000 ug/1 in soft and moderately hard water, based
primarily on effects on early life stages. Acute effects are observed in
a few species at the upper end of this range. Most freshwater aquatic
species experience acute effects in the range of 1-100 mg/1 total lead.
Aquatic organisms may be exposed to lead through water, diet and
sediment. The relative importance of these routes is highly variable
and depends on the species and the environment. Exposure is enhanced'
in the presence of high concentrations of lead, especially in soft,
acidic waters. Mean total lead concentrations were generally below
iU yg/l m 1979. However, concentrations of approximately 25,000 ug/1
which sometimes results in fish kills, have been reported near such
sources as an old smelter and a tailings pond. In addition, a concen-
tration of less than 1000 ug/1 resulted in a fish kill in 1970.
High concentrations of total lead (mean >50 ug/1, with ar least 20%
of the, observation levels >100 ug/1) have been found in the Catawba-Wate'ref
Basin, the James River, the Fox River-Wolf Creek drainage basin, and the
Kootenai River. Identifying areas with high aquatic exposures is difficult
because of analytical problems and the inherent problems with a^re-ations
of monitoring data. The identification of localized lead exposure areas
requires a more detailed investigation than was conducted here. In addi-
tion, the local conditions including pH, hardness, etc. great]y influence
toxicity. These factors have only been considered on a broad scale in
this analysis.
The data on lead toxicity in waterfowl, ducks, and gallinaceous
birds clearly indicate that ingestion of spent lead shot can be lethal;
numerous incidences of waterfowl mortality as a result of ingesting
spent lead shot have been reported. Waterfowl kills are more prevalent
in areas under heavy hunting pressure (such as the Mississippi Flyway)
and in lakes and marshes with hard bottoms, where lead shot can accumulate.
1.2 SOURCES OF LEAD TO THE ENVIRONMENT
In 1976, the supply of lead was approximately 1,515,000 kkg. About
34% of this supply resulted from domestic ore production, while about
35% resulted from secondary production. The remaining supply consisted
of imported ores and metals, and industry stocks.
Approximately 49% of the industrial supply was consumed in the
manufacture of lead-acid storage batteries and the production of battery
oxides. The production of antiknock gasoline additives consumed about
14% of the supply. The remaining 37% of the industrial supply was used
for such purposes as the production of red lead and litharge, ammunition,
solder, weights and ballast, pigments, cable covering, brass and bronze,
sheet lead, bearing metals, caulking metals, pipes, and type metal.
1-4
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Of the identified releases to the environment (-355,000-360,000 kkg),
53 % are airborne and 46% are in the form of solid waste. Known releases
to surface waters and POTWs account for less than 1% of the total.
Of the estimated 190,000 kkg lead released to the atmosphere, the
releases from the use of leaded gasoline comprise about 93%. Releases
from fossil fuel combustion, lead smelters, iron and steel production,
battery manufacture, and copper and zinc smelting, each contribute
about 1-2% of the total known airborne releases. However, some of
these sources may be important in local areas.
It was difficult to quantify releases of lead to water because of
large gaps in the data. However, aquatic discharges from the major uses
of lead are assumed to be small. Of the known releases to the aquatic
environment (800-950 kkg), 53%-63% are attributed to the iron and steel
industry, 21% to lead production, 6% each to battery production and the
nonferrous metal industry, and 4% each to the inorganic chemical and
pulp and paper industries. Urban runoff probably represents the major
source of lead to the aquatic environment, and perhaps as much as
21,000 kkg to surface waters and POTWs. However, these releases are
largely a result of the deposition of airborne releases.
Solid wastes represent a large source of lead (-165,000-163,000 kkg)
to the environment. Solid wastes are primarily produced as a result of
domestic ore production (34% of the known total), and ammunition use
(30% of the total). Other important sources include solder, weights
and ballast, bearing metals, and iron and steel production.
Numerous uncertainties exist in the materials balance for lead. The
releases from the production, use, and disposal of lead-acid storage
batteries are largely unknown, although lead-acid storage batteries
represent the single largest use of lead. In addition, releases from
other uses are unknown, and releases from relatively minor uses may be
of concern, although they are believed to be small compared with airborne
releases and solid waste.
1-3 FATE AND DISTRIBUTION OF LEAD IN THE ENVIRONMENT
Since the atmosphere receives the greatest portion of releases,
it is important to consider the fate of lead in this media. Transport
of lead in the atmosphere depends on particle size, chemical form, and
the distribution and height of the release. Particles larger than
20 ym are rapidly deposited. Although automobile exhaust, the largest
single source, contains lead in extremely small aerosol sizes, with a
mass median diameter of 0.5 pm or less, large particles may be released
during cold start or acceleration. These larger particles are deposited
onto the roadway, or within a few meters. Smaller particles also are
deposited, to some extent, near the roadway by impaction; however, some
fraction is carried a distance (-100 m) from heavily travelled roads
1-5
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and may be deposited by washout. Still, precipitation may carry some
of the particles a considerable distance; thus, more remote areas may
be contaminated.
Lead releases from smelter, fossil fuel combustion, and iron and
steel production are primarily from elevated point sources and are
generally less than 1 ym in size. Consequently, these particulates
are widely dispersed and are primarily deposited by precipitation.
Smelter emissions result in significant deposition of lead at distances
up to two miles from the smelter. Fugitive dusts account for higher
deposition near the source. Airborne releases from mining and milling
operations will largely be in the form of fugitive dusts, resulting in
localized deposition.
The deposited lead forms from all atmospheric sources are largely
insoluble. Lead accumulates in plants, leaf litter, and soil. Runoff
and erosion introduce lead into surface waters as a suspended solid,
which results in sediment concentration.
The monitoring data for lead generally reflect these fate pathways.
The range of lead levels in air for remote areas of the continental United
States is 0.0001-0.01 yg/m^. In contrast, urban areas show levels of
0.5-10 yg/rn^, which are considerably higher, primarily because of auto-
mobile use. The monitoring data show rapid deposition; and it has been
estimated that lead levels in air generally decrease by about 50%
between 10 and 20 meters from the highway.
Elevated atmospheric lead levels are also found in the vicinity of
point sources, such as smelters, in the range of 0.4-4 yg/m^. Consider-
ably higher levels have occasionally been reported, however.
Direct sources of lead to water are largely unidentified, although
probably relatively small. Lead reaching surface waters is likely to
be strongly sorbed onto suspended solids and sediments. Because lead
in the sediment is strongly sorbed, it is unlikely to be desorbed as a
result of a physical disturbance. Changes in the water chemistry, for
example, pH, could result in an increased solubilization of lead. Lead
found in the water column is expected to be strongly complexed by
organic molecules. Lead can bioconcentrate in aquatic organisms up to
2-4 orders of magnitude above water concentrations. It appears to be
fairly persistent in aquatic biota, with a lifetime of at least several
months. Little evidence suggests biomagnification of lead in aquatic
food chains.
Typical levels of lead in U.S. waters are less than 25 yg/1. Levels
of lead in seawater are considerably lower, on the order of 0.005 yg/1.
Lead concentrations in surface waters are higher in urban areas than
in rural areas.
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Sediments contain considerably higher levels of lead than surface
waters. Coastal lead sediment contains approximately 100 mg/kg, while
the average lead in river sediments was estimated to be about 20 mg/kg.
Higher concentrations were found in STORE! data, with mean concentra-
tions ranging from 27-267 mg/kg, during 1973-79.
Lead transported to soil is quite strongly sorbed, and, under most
conditions, is not subject to leaching. The movement of lead with the
erosion of soil particles is likely, however. Entrainment of soil
particles is also a possible route of lead transport. In addition,
uptake of lead into plants can occur, although only a small portion
of the total lead in any soil is available for plant uptake. Biocon-
centration factors are generally less than 1, although they may be
higher in the roots.
Monitoring data for lead in soils largely reflect airborne deposi-
tion patterns. An average concentration for lead in U.S. soils appears
to be about 20 mg/kg in uncontaminated soils. Elevated concentrations
are found in the vicinity of highways (up to 7600 mg/kg), and, in
general, in urban areas where a range of 100-800 mg/kg lead in soil is
found. Elevated concentrations are also found in the vicinity of
smelters (up to about 8000 mg/kg), in the vicinity of houses that at
one time were painted with lead-containing paints, and in old orchard
soils. Urban dust is also found to contain High levels of lead. Con-
centrations of about 1000-1600 mg/kg are found in urban residential
areas and 1400-2400 mg/kg in commercial areas.
1-7
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2.0 INTRODUCTION
The Office of Water Planning and Standards, Monitoring and Data
Support Division of the Environmental Protection Agency is conducting a
program to evaluate the exposure to and risk of 129 priority pollutants
in the nation's environment. The risks to be evaluated included potential
harm to human beings and deleterious effects on fish and other biota The
goal of the task under which this report has been prepared is to integrate
information on cultural and environmental flows of specific priority pollu-
tants and estimate exposure of receptors to these substances'. The results
are intended to serve as a basis for developing a suitable regulatory
strategy for reducing the risk, if such action is indicated.
This document is a brief assessment of the effects, exposure, and
potential risks that result from the production, use, release, and distri-
bution of lead. Numerous authors have noted a number of problems associated
with an analysis of lead. First, the literature on lead is voluminous and
could not be comprehensively reviewed within the time constraints of this
report. Therefore, previous reviews have been extensively used and have
been supplemented with information from the recent literature. Although
this may not be the most satisfactory approach, in general, it was deemed
the most appropriate and effective for the purposes of this report.
Second, the problems with analyses, and sample and laboratory contami-
nation have been widely acclaimed. Statements, in this report, have been
qualified on the basis of recent analytical data. However, older data,
and even recent data, can reflect this problem and could not be actively
addressed in this work.
Third, and perhaps most significant, regulatory mechanisms are
currently being effected for lead from many sources. Thus, exposure
estimates and conclusions can be expected to change over the next ten
years. This report attempts to point out which exposure routes will be
affected, and which exposure routes will continue to be a problem.
This report is organized as follows:
• Chapter 3.0 contains information on the production,
discharge, and disposal of lead.
• Chapter 4.0 describes available monitoring data and a
consideration of the fate of lead in five specific
pathways.
• Chapter 5.0 discusses the effects of lead on humans and
describes exposure scenarios.
• Chapter 6.0 considers the effects and exposure of biota
to lead.
• Chapter 7.0 discusses risk considerations for various
subpopulations of humans and biota.
2-1
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3.0 MATERIALS BALANCE
3.1 INTRODUCTION
Lead emissions to the environment may result from primary and
secondary production of lead and from the use of refined lead in manu-
factured products. In addition, the concentrations of lead that occur
naturally in the environment may cause inadvertent emissions as a result
of the processing of these materials. This section of the report has
been assimilated from four basic sources: government publications, trade
journals, standard references and text, and data published by the American
Bureau of Metal Statistics. This materials balance examines'releases of
lead to the environment of the United States for 1976.
Although more recent data are available for some of the use cate-
gories and for most of the production categories, the most accessible
and reliable literature is for 1974-76. The most definitive source of
information on lead emissions is Nriagu (1978), whose information and
assumptions are based on data for 1974 and 1975. Also, in considering
the ranges of uncertainty in the information available on lead uses and
emissions — typically an order of magnitude or more — attempts to scale
data for 1974 and 1976 to a later year, such as 1978, would require
adjustment factors that are small in comparison to the data uncertainties;
therefore, such adjustments seem unwarranted. In effect, the data
presented are approximately as reliable for any year between 1974 and
1978 as for the year 1976.
Lead is recovered from lead sulfide ores. In 1976, domestic mine
production was 518,000 kkg. The total primary U.S. smelter/refinery
production in that year was 597,000 kkg (domestic plus imported ores),
while secondary production (scrap processing) contributed 526,000 kkg to
the U.S. supply. Imports provided 79,000 kkg of ore and 129,000 kkg of
lead metal in 1976. Industry stocks (January 1) contributed 263,000 kkg,
which brought the total U.S. 1976 supply to 1,515,000 kkg. At the end of
1976, 5400 kkg of the supply was exported and 140,000 kkg remained in
industry stocks, leaving 1,370,000 kkg for industrial consumption.
Table 3-1 presents a summary of the lead supply, demand, and emissions.
Notes explaining the data in Table 3-1 are in Appendix A. Where firm
data were unavailable, estimates were based on engineering assumptions
about manufacturing and use processes.
Approximately 49% of the industrial supply was consumed in the
manufacture of lead-acid storage batteries and the production of battery
oxides. About 14% of the supply was consumed for the production of anti-
knock gasoline additives. The remaining 37% of the industrial supply
was used in twenty-two other categories. Figure 3-1 is a graphic repre-
sentation of the flow of lead from commerce and inadvertent sources to
the media.
3-1
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TABLE 3-1. SUMMARY OF U.S. LEAD SUPPLY, USE, AND EMISSIONS, 1976*
(kkg)
Production and Emissions
Domestic ore mining and milling,
smelting, and refining
Imported ores (smelting and refining)
Imported metals
Industry stocks, January 1
Secondary production
Uses and Emissions
Lead-acid storage batteries
(e.g., grids and posts)
Storage battery oxides
Gasoline antiknock additives
Red lead and litharge
Ammunition
Solder
Heights and ballast
Pigments
Cable covering
Brass and bronze
Sheet lead
Searing metals
Calking metals
Pipes (traps and bends)
Collapsible tubes
Type metal
Terne metal
Annealing
Miscellaneous chemicals
White lead
Lead plating
Casting metal
Galvanizing
Foil
Other
Exports, metal
Industry stocks, December 31
Inadvertent Emissions
Suoslv
518,000^
79.00091
129,000^
263,000®
526,000^
Consumption
348,000®
398,000®
217,000®
77,000®
66,000*2
57,OOoS
20,000®
15,000®
14,000®
14,000®
22,000®
12,000®
11,000®
13,000®
2,110*;
14,000^
1,400®
2,600®
'• 'uu^v
350®
6,080®
1.140*
*.«08
48,000^
5,440
140,000
Airborne
Emissions
820®
Aquatic
Discharges
MA.
180 S
MA
3-110©
Discharges
to POTWs
NA
10-4303
MA!
Solid
Vastes
MA
Combustion of oil
Combustion of coal
Iron and steel production
Copper and zinc smelting
Timber products
Leather tanning
Petroleum refining
Paint and ink manufacturing
Coal mining
Inorganic chemical manufacturing
Textiles
Pulp and paper
Rubber products
Laundries
Miscellaneous chemicals (pesticides) manufacturing
Nonferrous metals
Fertilizer (phosphatic)
POTW discharges
TOTAL 1,515,000 1,513,000
2.63C&2
48o£f
1,240®
1,800©
0
0
NA@
o
NA©
NA
0
-o
-o
0
NA
NA
" n^
60-960^
189,000-190,000
0
NA
5000
NA
-0
-0©
-00
0
NA0
10-500
100
400
NA5<
°X
NA®
500
MAX
10*^
800-950
0
0
5000
NA
-00
-00
-0®
-00
NA
40
100
100
o|t
.0©
5JA0
ioO
-0©
-
590-1,010
0
1,4300
3,73oC|
5,4000
NA
NA
-0
NA
HA©
NA
NA
NA
NA
0
NA
NA
95©
250-3,680^?
165,000-168,000
Note: MA - Not available
Numbers aay not add due to rounding.
Circled numbers refer to notes in Appendix A.
3-2
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1 .|iO-*&3 JTOi
STOCKS .AMUAN*
COMtUfTlOM Of Oil.
• STCli, MIGOUCTIO«I
'CMJ >»T>cigcs >•••:
FIGURE 3-1 ENVIRONMENTAL FLOW OF LEAD, 1976 (kkg)
3-3
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Of all estimated emissions of lead to the environment, 53% are
airborne and 47% go to land. Identified emissions to water and POTWs
account for <1% of all emissions. Emissions from the use of leaded
gasoline comprise over 93% of all airborne emissions of approximately
190,000 kkg. Although few sources of aquatic discharges were quantified,
aquatic discharges from iron and steel production are the primary source
of waterhome wastes, which amount to approximately 53-63% of aquatic
discharges. Solid wastes, which are primarily generated during mining
and beneficiation processes and as a result of ammunition use, contain
between 165,000 kkg and 168,000 kkg of lead.
3.2 PRODUCTION OF LEAD
Lead is recovered from naturally-occurring sulfide ores, which
typically contain between 1 and 6% lead. Zinc and, to a lesser extent,
other metal sulfides are often associated with lead sulfide. The domestic
lead production is comprised of primary and secondary (scrap) sources.
Six domestic smelters and five refineries processed 518,000 kkg of domes-
tically mined ores and 79,000 kkg of imported ores in 1976 (Nriagu 1978).
Capacities and locations of domestic lead smelters are presented in
Table 3-2. Approximately 85 companies operating 115 plants produce lead
and lead alloys for industrial use from recycled materials, principally
old batteries. Two companies, NL Industries and RSR Corporation, operate
about 18 secondary smelters; these smelters account for over one-half of
the total secondary lead production (U.S. Bureau of Mines 1977a).
Thirteen companies operating approximately 24 plants account for most
of the remaining secondary lead production (U.S. Bureau of Mines 1977a).
3.2.1 Primary Production
In 1963, vast deposits of lead ore were discovered in Missouri; and,
in 1976, Missouri contributed 82% of the total domestic production.
Idaho contributed 9%, Colorado 4%, and Utah 3%. The 25 leading mines
listed in Table 3-3 accounted for over 99% of the total U.S. production
(U.S. Bureau of Mines 1977b).
Prior to smelting, standard crushing, grinding, and flotation methods
are used to beneficiate lead ore at the mine site. To obtain the end
product, three operations take place at the smelter (U.S. Bureau of Mines
1977a).
• The ore concentrate is sintered with additional charge
material of recycled sinter, sand, and other inerts; this
process oxidizes the lead and sulfur when they change to
oxides and agglomerates the charge to form a dense perme-
able mass suitable for furnace feed.
• The lead oxide in the sinter is reduced to produce molten
lead.
• The resultant lead bullion is refined to eliminate impurities.
3-4
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1
1
1
1
1
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1
1
1
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1
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TABLE 3-2. CAPACITIES AND LOCATIONS
SMELTERS AND REFINERIES,
Company Location
Bunker Hill Bradley, IDa
St. Joe Minerals Herculaneum, M0a
AMAX Boss, MO3
ASARCO Glover, MO3
El Paso, TXb
h
East Helena, MT
h
Omaha, NE
E>enotes primary smelter and refinery.
ASARCO plants at El Paso, Texas and East Helena
smelters only. They supply feedstock to ASARCO
Omaha, Nebraska.
Source: U.S. Bureau of Mines (1977a).
3-5
OF U.S. LEAD
1977
Capacity
(kkg)
117,910
204,075
126,980
99,770
81,630
81,630
163,260
, Montana are
's refinery at
-------
TABLE 3-3. U.S. LEADING LEAD-PRODUCING MINES
IN ORDER OF OUTPUT, 1975
Mine
Buick
Fletcher
Magmont
Ozark
Brushy Creek
Viburnum #29
Viburnum #28
Bunker Hill
Lucky Friday
Indian Creek
Star Unit
Viburnum #27
Leadville Unit
Idarado
Bingin
Ontario
Sunnyside
Balmat
Pan American
Austinville and
Ivanhoe
Camp Bird
Emperius
Ground Hog
Pend Oreille
Eagle
County and State
Iron, MO
Reynolds, MO
Iron, MO
Reynolds, MO
Reynolds, MO
Washington, MO
Iron, MO
Shoshone, ID
Shoshone, ID
Washington, MO
Shoshone, ID
Crawford, MO
Lake, CO
Ouray & San Miguel, CO
Utah, UT
Summit, UT
San Juan, CO
St. Lawrence, NY
Lincoln, NV
Wythe, VA
Ouray, CO
Mineral, CO
Grant, NM
Pend Oreille, WA
Eagle, CO
Operator
AMAX Lead Co.
St. Joe Minerals Corp.
Cominco American, Inc.
Ozark Lead Co.
St. Joe Minerals Corp.
St. Joe Minerals Corp.
St. Joe Minerals Corp.
The Bunker Hill Co.
Hecla Mining Co.
St. Joe Minerals Co.
Hecla Mining Co.
St. Joe Minerals Co.
ASARCO, Inc.
Idarado Mining Co.
Kennecott Copper Co.
Park City Ventures
Standard Metals Corp.
St. Joe Minerals Corp.
St. Patrick Mining Co.
New Jersey Zinc Co.
Federal Resources Co.
Minerals Engineering Co,
ASARCO, Inc.
The Bunker Hill Co.
New Jersey Zinc Co.
Source: U.S. Bureau of Mines (1977b).
3-6
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Sintering is carried out in updraft sintering machines of a type
commonly used in the metals production industry. The lead oxide is then
reduced in a blast furnace that separates the charge into four layers:
slag, speiss (essentially arsenic and antimony), matte (mostly copper
and other metal sulfides), and product lead metal. The lead contains
varying amounts of other metals that are removed by refining.
Usually, copper dressing is the first step in refining. The bullion
is maintained above the melting point of lead but below the melting
point of copper. The copper begins to freeze and floats to the surface.
The scum floating on the surface is referred to as dross and is skimmed
and processed for metal recovery.
Other impurities, such as arsenic, antimony, tin, gold, and silver,
are removed by similar operations of melt-freeze cycles. The refining
process is complex and variable depending on the impurities present in
the original concentrate.
Emissions from Primary Production
Environmental emissions of lead from primary production are in the
form of particulate airborne emissions from mining, milling, and materials
handling operations; airborne emissions are also associated with blast
furnaces and dressing operations. However, in smelting and refining
operations, precautions are generally taken to control emissions. Parti-
culates in off-gas streams are cooled and treated by baghouses. Some
plants also use the off-gases to produce sulfuric acids. These mechanisms
effectively reduce a large portion of the airborne emissions of lead.
The total known airborne emissions from mining, milling, smelting, and
refining processes are estimated at 1500 kkg for 1976, for both domestic
ores and foreign ores that are smelted and refined domestically.
Aquatic discharges may result from the flotation beneficiation
process. Aquatic discharges are probably small when compared with other
emissions from primary production because lead metal and most lead com-
pounds have extremely low solubility in water. Based on the releases of
one plant, it has been estimated that losses of approximately 180 kkg
have resulted from smelting and refining operations.
Solid wastes from primary production occur as unrecovered metal in
mine tailings; however, from emission control systems, they occur as
sludges. The total estimated amount of solid wastes generated by primary
production from both foreign and domestic ores is 56,000 kkg.
Detailed explanations of the emissions associated with primary
production are given in Appendix A.
3.2.2 Secondary Production
The recovery of lead from scrap metal is a significant contributor
to the annual lead supply. In 1976, 526,000 kkg of lead (approximately
3-7
-------
35% of the total supply) was recovered from scrap. Nearly 70% of
secondary production of lead is derived from storage batteries (U.S.
Bureau of Mines 1977a).
The remaining 30% is composed of solder, type metals, drosses, and
residues. The processing procedure depends on the composition of the
scrap. In general, secondary lead production has three major phases.
Pretreatment involves crushing and breaking the scrap metal into
suitable sizes and smelting and refining of the crushed scrap.
Crushing of the scrap is normally accomplished by jaw crushers.
Smelting and refining operations are similar to the primary lead produc-
tion, except some plants employ reverberatory furnaces rather than blast
furnaces. In addition, secondary lead processors do not employ a
sintering step because (1) lead is present in oxide form in the scrap,
and (2) the scrap material contains essentially no sulfide.
Emissions from Secondary Production
Environmental emissions of lead from secondary production operations
are largely unquantifiable. Smelting and refining of secondarv lead is
estimated to generate 180 kkg of airborne lead. Data on aquatic dis-
charges and solid waste generation are unavailable.
«
3.3 USES OF LEAD
Refined lead has a minimum purity of 99.85% and is marketed in four
grades: (1) corroding lead, a designation used to describe lead of high
purity; (2) chemical lead, lead of high purity but not desilverized;
(3) acid-copper lead, made by adding copper to fully-refined lead; and
(4) common desilverized lead, a designation used for fully-refined
desilverized lead.
Over 49% of the total U.S. demand, 746,000 kkg, is used for the
production of lead storage batteries. Approximately 47% of this total
(348,000 kkg) is used for the production of the battery posts and grids.
The remaining 398,000 kkg is used in the manufacture of lead oxides that
is used in batteries (Lead Industries Association. Inc. 1978). The
life span of storage batteries is typically 2-4 years; almost: all the
spent batteries are reprocessed by secondary smelters to recover the
lead values. Recycled batteries are the major source of feedstock for
the secondary smelters.
The next largest use of lead is in the manufacture of gasoline
antiknock additives, tetraethyl-lead and, to a lesser extent, tetramethyl-
lead. The production of these additives consumed 217,000 kkg of lead
(approximately 14% of the total demand) in 1976. These additives are used
to increase the octane rating of gasolines. Except for a slight increase
in 1976, the consumption of lead for additive production has decreased
since 1972. Consumption of lead for automotive applications will probably
3-8
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continue to decrease because later model automobiles have catalytic
converters that preclude the use of leaded gasoline.
The remaining 37% of the lead consumed has many uses. The American
Bureau of Metal Statistics and the Lead Industries Association, Inc.
(American Bureau of Metal Statistics 1978) compiles annually a list of
twenty-two applications for the remaining 37% of the lead supply. None
of these applications consumes more than 5.5% of this supply. Use
patterns for 1965-76 are shown in Table 3-4.
One of the larger uses of lead is the production of red and white
lead used in paint pigments. In the past, lead-base paints were used
extensively; however, because of their toxicity, use has been restricted
to protective exterior coatings for bridges and ships or in applications
where lead-base paints are sealed with a nonlead paint coating.
Most of the remaining uses of lead are congruent with the properties
of the metal. Lead is dense, malleable, has a relatively low melting
point, and is almost insoluble in water. In addition, lead is highly
resistant to corrosive chemicals and high frequency electromagnetic
radiation and it has good lubricative properties. Consequently, it is
used for weights and ballast in sailboats and for fishing tackle and also
for ammunition and ordnance.
Lead is a soft metal; thus it is amenable to uses such as solder-
ing and calking metals. Collapsible tubes for material packaging, such
as artists' paints, are made of lead, particularly if the material is
corrosive. For use in structural applications, lead must be alloyed with
other metals to increase its strength and hardness. Terne metals
(ternary lead alloys) are used in structural applications. Other
alloys include type metal, used in the printing industry, casting metal
and specialized brass and bronze alloys.
Because lead is relatively insoluble in water, it has been used for
plumbing pipes; recently, however, this use has become specialized and
more limited to applications where lead's corrosive resistant property
is important. Lead or lead alloys are used for piping and process vessels
in the chemical process and other industries where the handling of corro-
sive fluids is necessary. Lead or its alloys are also used for cable
sheathing, galvanizing, and electroplating.
Sheet lead is used for radiation shielding in hospitals and nuclear
plants. Lead foil is often used for the transport of radioactive material.
Because lead has good lubricative properties, it is used for bearings and
in specialized alloys. Lead chemicals are used in pesticides and for
glazing operations in the glass and ceramic industry. Environmental
emissions from these sources (see Appendix A) result from the volatiliza-
tion, leaching, or disposal of lead or lead bearing materials (U.S. Bureau
of Mines 1977a).
3-9
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TABLE .1-4. U.S. SUI'I'I.Y AND DKMANI) KKLATIONSHII'S OK LKAII. 1965-76
U>
Components of U.S. Supply
lloine.sl ic Ores
(•'orei^D Ores
SecoiuLiry (Scrap)
Saleb t>l CuvL Stockpile
Imports, Melal
Industry Stocks .Ian. 1
TOTAL
Distriluit I on ol Supply
Industry Slock;, Due. Jl
Export.-!. Mel.il
TOTAL INDUSTRY DEMAND
Kiul ll.ii1 DuuLind Pattern
Casoline Additives (SIC 2911)
Transportation (SIC 1691, 37)
Const rue I ion (SIC 344)
I'.iints (SIC 2851)
Ammunition (SIC 148)
Electrical (SIC 3356, 3357, 3691)
III her
TOTAL
1965
279,356
106,119
449,872
48,071
202,261
179,586
1,265,265
175,051
7,256
1.082,958
204,075
354,637
124,259
98,863
51,699
85,258
164,167
.[966
294,775
115,189
4)9,895
58,048
258,496
175,050
1.341,453
186,842
4,535
1,150,076
224,029
366.428
119,724
108,840
70,746
92,514
167,795
1967
239,448
113,375
432,619
25, 396
330,148
186,842
1, 127,848
209,517
6, 149
1,111,982
224,029
357, 158
108,840
91,421
71,653
88,886
167,795
19h8
1)1.055
110.654
427.197
26,303
106,566
209,517
1,411.292
15 j.28)
7,256
1 ,250,75)
2 17,6)4
410,8/1
106,1 19
99,7/0
74,) 74
78,909
241,076
1969
476,175
117,910
468,012
19,954
253,05)
151,28)
1 ,488, 187
206 , 796
4,5)5
1,277,056
245, 797
446.244
107,93)
92,514
71,651
87,072
225,84 3
1970
487,059
127,887
458,942
10,884
222,215
206 , 796
1 , 5 1 3 , 78 )
295,682
7,256
1,210,845
25 1,05)
497,0)6
109.747
89 , 79 )
6(>.2I 1
78,909
1 16,096
1971
5 1O.595
7), 467
444,410
9,070
175,051
295.682
1 ,528,295
224,029
5,442
1 ,298,824
2 )9,448
566,875
90,700
7 1,467
79,H|(,
1 18,81 7
129,701
1*7?
528,781
95,2)5
451,686
40,815
221,122
224,029
1,561,668
239,448
7,256
1.31 (.,964
251,05)
605,876
79,816
80.72)
77,095
116, 096
104,305
1 9/3
522,4 12
100,677
488,8/3
191 ,377
161 ,446
2)9,448
I ,704,25)
194,098
60,769
1 ,449, 186
248,518
6 )4 , 900
78 . 909
98 , 86 )
7), 467
122,445
192,284
1974
5)1 ,502
87,9/9
545, 107
241,262
IO/.02I,
194,098
1 , /(Id. 9 74
261,216
56 , 2 )4
1 , 189,524
226,750
711 ,995
70.746
105,212
78,909
12(1,6 II
75,281
|.,7',
482.',.'.',
96,14.'
51 1 ,548
l>, t48
89 , 79 1
21,1 . 'I/
,,,47.57.
26 1.0 III
19,047
1 , 11,5,49',
189,561
624, OK,
62, ',8 1
71.651
68,02',
68,9 12
80,72 1
19/6
5 1 7 . H>, .
78.9(19
526, 06O
0
I2H./94
21,1,0 IO
1 , 514.. 6 911
1 I9,((/H
5,442
1 , 169,5/0
•I7,4i,l
/I il, 1111
4 >. I'.n
96, 142
Mi, /I 1
1 16, (I'M,
II M.I 29
1,082,958 1,150,076 1,111,982 1,2',0.75) 1,277.056 I.2IO.845 1,298,824 1,316,964 1,449,186 l.)89.524 I.I65.V.5 ,,
Source: U.S. Bureau of Mines (1977a); American Bureau of Metal Statistics (1978).
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3.3.1 Emissions from the Use of Lead
Although batteries account for a large portion of lead use, they
are enclosed packages of lead; thus, none of this lead escapes into the
environment during use (Hepple 1971). However, limited data substantiate
that airborne and aquatic emissions have been estimated to be 1700 and
3-110 kkg, respectively, during the manufacture of batteries (see
Appendix A, notes 6 and 35). Solid waste discharges are thought to be
insignificant because of recycling.
The single largest anthropogenic environmental discharge of lead
results from the use of organic lead compounds as antiknock additives
in gasoline. Approximately 176,000 kkg of airborne lead emissions occur
annually from the combustion of gasoline. This source comprises over 93%
of the airborne lead emissions from all sources.
Aquatic discharges of lead from use activities are not well defined.
Lead discharges to the aquatic media are not believed to be significant
because lead and most lead compounds have extremely low solubility in
water. The only known aquatic discharges from use activities are derived
from pigment manufacture and are estimated to be approximately 15 kkg.
In addition, an estimated 45 kkg of lead are discharged to POTWs from
pigment production.
Solid waste results from the disposal of lead or lead bearing
materials or from nonreusable products, such as ammunition and ordnance.
Ammunition and ordnance are the largest contributors of solid waste from
lead use activities. They contributed about 50,000 kkg in 1976, which
is about 51% of all identified solid waste emissions from use activities.
Other important sources include lost and discarded weights and ballasts
(-10,000 kkg), discarded bearings (-9500 kkg), and spent soldering metals
(-5700 kkg). Other sources of solid waste from the lead use categories
and from lead bearing materials are summarized in Table 3-1 and Figure 3-1
Gathering of data and estimates is detailed in Appendix A.
3.3.2 Inadvertent Sources of Lead Emissions
At low level concentrations, lead is ubiquitous in the biosphere.
It occurs naturally in virtually every mineral and many organisms. The
processing of these materials may result in lead emissions because of
its presence in these materials. This is particularly true if large
quantities of the material are processed. For example, the combustion
of fossil fuels and smelting of other important metals result in anthro-
pogenic environmental discharges of lead. Lead and lead chemicals are
present in some products that are used by industry in their material
processing. Most of the important sources of lead, where lead is
inadvertently discharged, are presented in Table 3-1 and Figure 3-1.
Urban runoff is likely to be an important source of lead to aquatic
environments. In stormwater runoff from one city, lead concentrations
ranged from 0.1-2.85 mg/1, with a mean concentration of 0.46 mg/1
3-11
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(U.S. EPA 1974). Similarly. Bennett and coworkers (1981) reported
levels of approximately 1 mg/1 in stormwater and snowmelt runoff from
Boulder, Colorado.
Considerable other data on levels of lead in urban runoff will not
be reviewed here because it is extremely difficult to choose a represen-
tative concentration. For example, assuming a concentration of 1 mg/1
and a runoff volume of 21xlQl2 l/yr (U.S. EPA 1977), a loading of
21,000 kkg may be estimated. About 82% of this, or 17,000 kkg, would
go directly to surface waters, while about 4000 kkg would go to POTWs.
Even though this is a rough estimate, it does represent the largest
source to aquatic environments. This value, however, is not shown in
Table 3-1 or Figure 3-1, because it is believed to be largely attributable
to airborne releases.
3.4 FUTURE PROJECTIONS FOR LEAD
The U.S. Bureau of Mines (1977a) has projected an annual growth rate
of 1.8% for lead production and consumption through the year 2000. The
growth areas of lead by end use pattern are presented in Table 3-5.
The largest area of growth is expected to be in the transportation
industry (U.S. Bureau of Mines 1977a). Except for gasoline additives,
all other areas are expected to show modest growth. Leaded gasoline
additives are currently being phased out because of the large amount of
airborne emissions from motor-powered vehicles. Factors that could
retard domestic growth in lead production include shortage of skilled
labor, energy shortages, environmental restrictions, and the shortage of
investment funds at moderate cost in a capital intensive industry. The
latter two may have significant impact. Modifying existing smelters and
refineries in order to comply with the new regulations established by the
U.S. EPA and OSHA could cost the lead industry as much as $650 million by
1982 (Krammer 1978). It is possible that the stricter standards may
force some producers to shut down their operations, which will necessi-
tate the importation of a greater volume of lead.
Domestic reserves of high grade lead ore are primarily located in
Missouri (72.5% of domestic reserves). The known worldwide reserves
total 124 million kkg and are adequate to meet the world demand through
the year 2000 (U.S. Bureau of Mines 1977a). A summary of the worldwide
reserves is presented in Table 3-6.
3.5 SUMMARY
In 1976, domestic mine production of lead was about 518,000 kkg.
The total primary U.S. smelter/refinery production was 597.000 kkg
(domestic plus imported ores), while secondary production (scrap
processing) contributed 526,000 kkg to the U.S. supply. Approximately
49% of the industrial supply was consumed in the manufacture of lead-
acid storage batteries and the production of battery oxides. About 14%
of the supply was consumed for the production of antiknock gasoline
3-12
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I
_ TABLE 3-5. U.S. FORECASTS FOR LEAD DEMAND, 1976 and 2000
I
• Production (Demand
Primary
• Secondary
_ End Uses
™ Gasoline Additives
• Transportation
Construction
| Paints
• Ammunition
Electrical
• Other
• Source: U.S. Bureau of Mines (1977a).
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1976
843,510
526,060
217,461
710,181
45,350
96,142
66,211
116,096
118,129
Forecast Range, 2000
934,210
616,760
36,280
1,106,540
45,350
81,630
54,420
63,430
90,700
2,122,380
1,251,660
181,400
2,31.2,850
136,050
154,190
136,050
181,400
272,100
Probable
1,333,290
780,020
72,560
1,514,690
63,490
117,910
81,630
136,050
126,980
3-13
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TABLE 3-6. SUMMARY OF WORLD LEAD RESERVES
North America
United States
Canada
Mexico
Other
Total
South America
Brazil
Peru
Other
Total
Europe
W. Germany
Bulgaria
Yugoslavia
Spain
Poland
Sweden
Other
Total
Africa
Morocco
S.W. Africa
Algeria
S. Africa
Other
Total
Reserve
25.8
11.7
4.1
.!_
42.3
2.4
3.2
1.7
7.3
4.1
2.7
2.7
3.0
2.3
2.3
5.6
22.7
1.4
1.4
.6
5.1
1.3
9.8
Other
45 = 9
18.2
5.0
1.1
70.2
2.2
4.1
1.9
8.2
5.0
2.7
2.7
3.4
3.2
1.4
5.3
23.7
1.4
2.3
2.1
4.0
2.4
12.2
Total
71.7
29.9
9.1
1.8
112.5
4.6
7.3
3.6
15.5
9.1
5.4
5.4
6.4
5.5
3.7
10.9
46.4
2.8
3.7
2.7
9.1
3.7
22.0
Asia
U.S.S.R. 16.3
Peoples Republic of China
Iran 1.8
Other 4.0
Total 24.8
Oceania: Australia 17.1
World Total 124.0
16.3
1.8
3.3
24.1
14.7
153.1
32.6
3.6
7.3
48.9
31.7
277.0
pleasured and indicated.
Includes inferred and hypothetical resources,
Source: Kirk-Othmer (1967).
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additives. Other important use categories include red lead and litharge
(5%), ammunition (4%), and solder (4%). The remaining 15% is divided
among eighteen use categories. Each of the categories represents about
1% or less of the total supply, while about 9% is contained in industry
stocks.
Of the identified releases of lead to the environment (355,000-
360,000 kkg), about 53% was airborne and 46% was in the form of solid
waste. Less than 1% of the total releases was identified as being re-
leased to surface waters or POTWs.
Of the estimated 190,000 kkg of lead released to the atmosphere,
93% was attributed to the use of gasoline antiknock additives. These
releases are widely distributed; however, they are more concentrated in
urban or heavily trafficked areas. Approximately 2% of the identified
releases was attributed to fossil fuel combustion, and about 1% each to
lead production, battery manufacture, copper and zinc smelting, and iron
and steel manufacture.
The identified releases to the aquatic environment are relatively
low (800-950 kkg). Of these, 53-63% was attributed to iron and steel"
production, 21% to lead production, 6% each to battery production and the
nonferrous metal industry, and 4% each to the inorganic chemical and
the pulp and paper industries. The remaining 2% of identified releases
was attributed to pigment manufacture, the textile industry, and POTW
discharges.
Solid wastes represent a large portion (165,000-168,000 kkg) of the
total releases of lead to the environment. Lead production accounts for
a large portion of these releases (34%) as well, and ammunition use could
account for about 30%. Other important sources include solder, weights
and ballast, bearing metals, and iron and steel production.
There are numerous uncertainties in the materials balance for lead
The releases from the production, use, and disposal of lead-acid storage
batteries are largely unknown, although this is the largest single use°
of lead. In addition, releases from other uses, although minor, may be
significant. The releases from several sources are largely unknown or
have only been roughly estimated; however, they may be significant on a
local scale. The lack of data on which to estimate aquatic releases in
general is of concern. Although they are likely to be low when compared
with airborne releases and solid wastes, they may be significant on a
local scale.
Urban runoff probably represents the major source to aquatic environ-
ment. Estimates are not shown in the materials balance (Table 3-1)
because these releases represent an indirect source of atmospheric
emissions. However, this source may represent as much as 21,000 kkg of
lead discharging to surface waters and POTWs.
3-15
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REFERENCES
American Bureau of Metal Statistics. Non-ferrous metal data. New York
NY: American Bureau of Metal Statistics; 1978. '
Bennett, E.R.; Linstedt, K.D.; Nilsgard, V.; Battaglia, G.M.; Pontius, F.W.
Urban snowmelt — characteristics and treatment. J. WPCF 53(1) -.119-125;
X 7 O J. •
enVir°nment' Essex' En§land: Applied Science
Kirk-Othmer. Encyclopedia of chemical technology. Vol. 12. New York NY-
Interscience Publications; 1967. ' ' '
Krammer, L. New EPA lead standard could cost $650 million. Washington
Post; October 1, 1978.
Lead Industries Association, Inc. U.S. lead industry 1977 annual review.
New York, NY: Lead Industries Association, Inc.; 1978.
Nriagu, J.O. The biogeochemistry of lead in the environment. Part A
Amsterdam: Elsevier; 1978.
U.S. Bureau of Mines. Mineral commodity profiles. Washington, DC:
Bureau of Mines, U.S. Department of the Interior; 1977a.
U.S. Bureau of Mines. Minerals yearbook metals. Vol. 1, Minerals and
fuels. Washington, DC: Bureau of Mines. U.S. Department of the Interior;
U.S. Environmental Protection Agency (U.S. EPA). Background information
for new source performance standards, primary copper, zinc, and lead
smelters. Vol. 1: Proposed standards. EPA 440/2-74-002a. Washington,
DC: U.S. Environmental Protection Agency; 1974.
U.S. Environmental Protection Agency (U.S. EPA). Nationwide evaluation
of combined sewer overflows and urban stormwater discharges. Vols I and
II. EPA Report No. 40 CFR 403. Washington, DC: U.S. Environmental
Protection Agency; 1977.
3-16
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4.0 FATE AND DISTRIBUTION OF LEAD IN THE ENVIRONMENT
4.1 INTRODUCTION
This chapter describes the levels of lead that have been observed
in the environment and the environmental pathways that may result in
these levels. Extensive data support these areas. Here, however, only
the major topics will be discussed, including summaries of the available
data.
4.2 DISTRIBUTION OF LEAD IN THE ENVIRONMENT
There is a large data base concerning the concentrations of lead
in the environment. Nriagu (1978a,b) and Chow (1978) have reviewed the
literature extensively. The following discussion is meant to address
the key points and to briefly review concentrations of lead that are
found in the United States.
4.2.1 Water and Sediment
4.2.1.1 Freshwater
Patterson (1965) estimated that the background level in surface
waters during preindustrial times was 0.5 yg/1. Current global levels
of lead in water are 1-10 yg/1 (Livingston 1964).
Anthropogenic sources are industrial discharge, fallout, washout,
and runoff, with the primary source being lead emitted to the air as a
result of automobile use. Fleischer (1973) has estimated that these
anthropogenic sources account for over 90% of the lead in U.S. surface
waters.
Typical lead levels in U.S. surface waters are less than 25 yg/1.
Lead concentrations were detected in 63% of the samples at a range from
1-55 ug/1 with an average of 3.9 yg/1 in a study of 749 locations (Durum
JL£. al. 1971) and Kopp (1969) reported a mean concentration of 23 yg/1 in
water sampled from 130 stations across the United States. This is a mean
of the positive values and lead was detected in 19% of the 1580 samples.)
Bradford (1971) reported an average concentration of 3 yg/1 in California
surface waters (ranging from <0.5 yg/1 to 25 yg/1). Mathis and Cummings
(1973) found a range of 1-18 yg/1 in the Illinois River and Mancy (1971)
reported a range of 0.6-3.3 yg/1 in the Great Lakes. Levels of lead in
surface waters and sediment are summarized in Tables 4-1 and 4-2.
4.2.1.2 Seawater
Seawater generally contains low levels of lead. Settle and Patterson (1980)
estimate that prehistoric lead levels in the ocean were 0.0005 ug/1 and report
that present day levels are 0.005 yg/1. For nearshore potentially contami-
nated waters, Patterson (1974) reported levels of 0.014-0.08 ug/1 off the
Southern California coast. Patterson _et _al. (1976) found similar results
on the east coast: 0.02-0.04 yg/1 in Georgia, and 0.14 ug/1 in the Long
4-1
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TABLE 4-1. CONCENTRATIONS OF LEAD IN WATER
Description
Background
Global level
U.S.
U.S.
Stream near smelter — MO
Surface waters — CA
Illinois River
Great Lakes
Rainwater — U.S. Urban
Rainwater — CA Urban
Rainwater — NH Rural
Rainwater — NB
Snow — NB Rural
Seawater — Background
Seawater — Present day
Nearshore contaminated (CA)
Nearshore contaminated (GA)
Nearshore contaminated (L.I. Sound)
Groundwater — MO
Groundwater — CA
Storm runoff — NC
Storm runoff
ConceiU ja t i on
Mean
Range
0.5
3.9
23
300
3
36
38
1-10
1-55
2-140
0.5-25
1-J8
0.6-3.3
13.4
4.3
7.8
0.0005
0.005
0.14
3
1500
5500
0.014-0.08
0.02-0.04
2.9-3.8
0.5-10
]00-]2,000
jte_f erencei
Patterson (1965)
Livingston (1964
Durum et al. (1971)
Kopp and Kroner (1967), Kopp (1969)
Gale and Wixson (1979)
Bradford (1971)
Mathis and Cummings (1973)
Mancy (1971)
Lazarus et al. (1970)
Chow and Earl (1970)
Schlesinger e^ al. (1974)
Struempler (1976)
Struempler (1976)
Settle and Patterson (1980)
Settle and Patterson (1980)
Patterson (1974)
Patterson et al. (1976)
Patterson ^t al. (1976)
Proctor £t ajL. (1974)
Bradford (1971)
Bryan (1974)
Newton et al. (1974)
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TABLE 4-2. CONCENTRATIONS OF LEAD IN SEDIMENT
u>
Description
Coastal sediment
California Coast — Surface
California Coast — Lower levels
Great Lakes — Surface
Great Lakes — Lower level
Wisconsin Lakes — Surface
Wisconsin Lakes — Lower level
River sediment
U.S. — 1973-79
Concent rat uni
Mean
87
30-50
10
109
28
918
48.8
23
27-267
Range
1-912
Reference^
Nriagu (1978a)
Chow jet ai_. (1973)
Chow jat al. (1973)
b
h
Fitchko and HutchJuson (J975)
d.S. MI'A (1980)
Thomas (1976), Edgington and Robbins (1976), Kemp and Dell (1976).
Peterson (1973), Iskander and Keeney (1974)
-------
Island Sound, NY. Both Patterson (1974) and Settle and Patterson (1980)
believe that most studies, before 1970, overstated the concentration of
lead in ocean water by as much as an order of magnitude.
4.2.1.3 Rainfall
In some situations, rainfall appears to contain relatively high
levels of lead. Lazarus e_t al. (1970) correlated the consumption of
gasoline with concentrations of lead in rainwater collected nationally
at 32 urban stations. They found an average level of 36 ug/1, which
agrees with a study by Chow and Earl (1970) that reported an average
concentration of 38 ug/1 in rainwater collected at San Diego, CA.
Schlesinger _et al. (1974) measured lead concentrations in the precipita-
tion of a rural area in New Hampshire. Their measurements, an average
of 13.4 ug/1, showed lower levels than those found in urban settings.
Struempler (1976) reported an even lower lead content, an average of
4.3 ug/1, in rainwater collected in rural areas of Nebraska in 1973;
snowfalls in the same area were slightly higher, with a mean value of
7.8 ug/1.
4.2.1.4 Urban Runoff
Extremely high levels of lead have been reported in urban runoff.
Bryan (1974) reported levels in Durham, NC runoff, ranging from 100 ug/1
to 12,000 ug/1, with an average of 1500 ug/1. Newton and co-workers
(1974) compared levels up to 5500 ug/1 with a concentration of only
90 ug/1 in an open field. Although these are unusually high levels for
most water bodies, Kopp and Kroner (1967) reported levels ranging from
80-200 ug/1 in the Mississippi River.
4.2.1.5 STORET Data
The STORET Water Quality System contains a large amount of monitoring
data on lead. Because of the size of the data base, only detectable levels
were used in the following analysis. These data comprise roughly 60% of
all total lead observations for the period considered here — 1970-79.
Thus, the mean values discussed below are actually means of the detected
values.
Lead concentrations in ambient waters appear to have declined in the
United States since 1970. Figure 4-1 illustrates the trend of lead con-
centrations from 1970 to 1979. From 1970 through 1973, mean concentration
decreased to 70 ug/1; to date, it has fallen below 40 ug/1. It is
impossible to say whether these results reflect an actual decline or
change in analytical methodology or detection limits.
To observe regional variations of lead concentrations, the data were
disaggregated to the major basin level. Most major basins across the
country reported mean values >50 ug/1, from 1970 to 1972; however, in
4-4
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100
90
80
_ 70
•3 60
5
1 50
§ 40
5
0 30
20
10
Mean
_L
-L
_L
JL
_L
1970 1971 1972 1973
1974 1975
Year
1976 1977 1978 1979
FIGURE 4-1 MEAN AMBIENT VALUES OF LEAD CONCENTRATIONS
IN U.S. SURFACE WATERS, 1970-79 (DETECTED LEVELS
ONLY)
4-5
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more recent years, the conditions have altered. Since 1973, mean values
for major river basins in the East, South and Midwest have been <50 ug/1.
The higher concentrations of lead appear in the western regions of the
country, specifically in the Pacific Northwest and California basins.
In the Pacific Northwest basin, mean concentrations, from 1970 to 1973,
fluctuated between 133-336 ug/1. In 1976, concentrations decreased,
resulting in a mean value of 127 ug/l. Mean levels have declined annu-
ally since 1976 to 69 yg/1 in 1977, to 61 ug/1 in 1978, and to 32 -g/1
in 1979. Similarly, for the California basin, mean concentrations of
lead in the early portion of the time period appeared in the range
80-228 Ug/1. A decline has occurred annually from a mean level of
105 uS/1 in 1976 to 43 ug/1 in 1979.
The literature indicates higher concentrations of lead near highways,
in urban areas, and, in general, where traffic is heaviest. Retrievals'
from STORET were used to contrast urban and rural lead concentrations.
Areas in the East, Midwest, and West were selected and data were aggre-
gated by county.
Retrievals from STORET were consistent with the literature. Mean lead
concentrations in counties that were mostly urban, on the average, were
fifteen times higher than the mean concentrations of rural counties.
For instance, in New York, the urban county of Nassau was contrasted
with Madison and Steuben counties of upstate New York. In Nassau county,
mean concentrations were in the range of 13-65 ug/1, with maximum levels
from 37 to 300 ug/1. In Madison and Steuben counties, the mean and
maximum concentrations ranged from undetected to 14 ug/1 and undetected to
37 ug/1, respectively. Similar results appeared for Los Angeles when
contrasted with Fresno and Kern counties and for Cook county (Chicago, IL)
contrasted with the rural counties of Livingston, Shelby, and Whiteside.
Table 4-3 presents the urban and rural lead concentration results.
4.2.1.6 Lead in Sediment
In aquatic environments, lead is found at much higher concentrations
in the sediment than in the water column. In coastal sediment, lead
concentrations range from 1 mg/kg to 912 mg/kg with a mean value of
87 mg/kg (Nriagu 1978a). The highest concentrations remain in the surface
layer; Chow et al. (1973) reported an average of 10 mg/kg in deep layers
on the California coast compared with levels of 30, 29, and 50 mg/kg on
the surface. The average concentration for the Great Lakes was 109 mg/kg
at the surface and 28 mg/kg in the deeper layers (Thomas 1976, Edgington
and Robbins 1976, Kemp and Dell 1976). The mean concentrations for a
sampling of lakes in Wisconsin were 918 mg/kg in the surface layer and
49 mg/kg in the deeper layers (Peterson 1973, Iskander and Keeney 1974).
The surface layers appear to contain three to five times the concentration
of lead as deeper layers (see Table 4-2).
Fitchko and Hutchinson (1975) have estimated the average concentra-
tion of lead in river sediments to be 23 mg/kg. Nriagu ("19783) has
4-6
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TABLE 4-3. MEAN AND MAXIMUM RANGES OF LEAD CONCENTRATIONS
IN AMBIENT SURFACE WATERS OF URBAN AND RURAL AREAS
Urban/Rural Counties
East - New York
Nassau (urban)
Madison (rural)
Steuben (urban/rural)
Midwest - Illinois
Cook (urban
Livingston (rural)
Shelby (rural)
Whiteside (urban/rural)
West - California
Los Angeles (urban)
Fresno (urban/rural)
Kern (urban/rural)
Concentrations (ug/1)'
Maximum Range
37-300
ND-4
4-37
20-1700
ND-40
ND-10
10-20
178-2400
ND-370
1-45
Mean Range
13-65
ND-3
2-14
15-71
ND-8
ND-1
1-5
53-309
ND-89
1-29
Note: ND
a
not detected.
Ranges generally include detectable levels only, except where ND is
indicated.
Source: U.S. EPA (1980).
4-7
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estimated lead levels in polluted environments at about four times this
value, 98 tag/kg.
In the STORE! data base, lead concentrations in sediment have been
recorded in only one-third of the major river basins, mainly in the East
and Midwest. Over a 7-year period, 1973-79, maximum concentrations of
lead in sediment ranged from 440-1000 mg/kg and mean concentrations
from 27-267 mg/kg. In general, lead concentrations in sediment are two
to three orders of magnitude higher than lead concentrations in ambient
waters (U.S. EPA 1980).
4.2.2 Air
Nriagu (1978b) has an extensive discussion on the levels and forms
of lead in the atmosphere; thus, they will only be discussed briefly
here.
Background lead levels are present in the atmosphere (Table 4-4)
as the result of releases from natural sources, including windblown dust,
plant exudates, forest fires, vulcanism and radioactive decay (Nriagu
1978b). Using geochemical evidence, Patterson (1965) estimated the pre-
industrial levels of lead in the atmosphere to be approximately 0.6 ng/m3.
This figure is an order of magnitude lower than the'lowest level reported'
for the continental United States (8 ng/m3). Chow et. al. (1972) reported
this level at 3800 meters at a relatively uninhabited site. The range of
lead levels for remote areas of the continental United States is
0.1-10 ng/m-> (Nriagu 1978b).
According to Nriagu (I978b), lead released to the atmosphere by
natural sources accounts for only a small percentage, approximately 4%,
with the remaining 96% accounted for by anthropogenic sources. In air,'
the primary anthropogenic sources of lead are internal combustion engines,
lead smelting, and steel production.
Lead concentrations are greater in urban or more developed areas.
Nriagu (1978b) reported an average range of 0.5-10 ug/m3 in the developed
areas, 0.1-1 ug/mj in more rural areas, and <0.01 ug/m3 in locations
distant from developed areas. Measurements of concentrations in the
immediate vicinity of traffic movement were usually found to exceed
10 ug/m . For the United States, urban lead concentrations ranged from
a relatively low level of 0.14 yg/m3 reported for Los Alamos by Tepper
and Levin (1972) to a high of 7.5 ug/m3 reported in mid-Manhattan by Chow
(1973). Data collected in the U.S. EPA's National Air Sampling Net-
work (NASN), during 1966 and 1967, showed average urban levels of
1.1 ug/m-3. Nonurban areas averaged 0.21 yg/m3 near the city, .096 yg/m3
at increasing distances from cities, and 0.022 yg/m3 in remote rural
areas (McMullen et al. 1970). These data indicate an average urban
level almost ten times higher than concentrations found in rural settings.
The correlation between atmospheric lead concentrations and auto-
mobile usage is supported by data indicating increased levels paralleling
4-8
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TABLE 4-4. CONCENTRATIONS OF LKA1) IN TliE ATMOSPHERE
Description
Baseline-preIndus trial
Lowest level — Continental U.S.
(White Mountains, CA)
Global — Urban
Global — Rural
Global — Remote
Boston — Spring
Boston — Winter
Montana — Near smelter
Montana — Distant from smelter
Idaho — Near smelter
Concentration (jig/m )
0.0006
0.008
3.9
5.4
0.5-10
0.1-1
0.0001-0.01
147.9
0.4-4
0.1-0.7
60-254
Reference
Patterson (1965)
Chow et uj. (1972)
Nriagu (1978b)
Nriagu (I978b)
Nriagu (1978b)
O'Brien et ;U. (1975)
O'Brien et al. (1975)
U.S. EPA (1972)
U.S. EPA (1972)
Rayaini e^t al. (1977)
-------
increases in gas consumption. Chow (1973) examined both the 1961-1962
Tri-City Project conducted in Los Angeles, Philadelphia and Cincinnati
and the 1968-1969 Seven-Cities Project conducted in the above cities
and additionally New York, Chicago, Houston, and Washington, DC, and
found significant increases in lead concentrations over that time period.
Los Angeles had the highest increase, 56%, with smaller increases of
19% in Philadelphia and 17% in Cincinnati.
Seasonal trends in atmospheric lead levels based on both automobile
usage patterns and climate conditions are also discussed in the literature.
A 1972 study by O'Brien eg al. (1975) shows a variation from 3.9 yg/m
in the spring to 5^.4 yg/m in the winter in Boston. Colucci ej^ al. (1969)
reported 4.9 ug/m in the spring and 10.3 yg/m in winter in the~960-65
Los Angeles Study. These studies indicate a possible average seasonal
variation of over 50%.
A large proportion of lead emitted in automobile exhaust settles
quickly in the vicinity of the source. Nriagu (1978b) states that lead
levels in the atmosphere generally decrease by about 50% between 10 and
50 meters from highways. Lead concentrations also decrease sharply with
increased height from the street level. Schroeder (1974) reported levels
of 14.3 yg/m3 at 0.61 meter, 8.3 ug/tn3 at 1.5 meters, and 5.1 yg/m3 at
0.2 meter.
In addition to the impact of automobiles in urban areas, local
point sources also contribute to levels of lead in the atmosphere. The
U.S. EPA (1972) measured lead levels in East Helena, Ml, which contains
an industrial smelter complex; in 1969, concentrations ranged from
0.4-4 yg/m3 depending on the distance from the plant. The maximum daily
concentration was 15 yg/m3. In neighboring Helena, MT, in 1969, an
average daily concentration of 0.1 yg/m3 up to a maximum of 0.7 yg/m3
was reported. In 1976, Ragaini and co-workers (1977) conducted a study
in Kellogg, ID, near a lead smelting complex. Air samples taken at the
town hall ranged from 60-254 yg/m3, with a mean value of 147.9 yg/m3.
4.2.3 Soil
All soils contain detectable levels of lead, ranging in concentra-
tion from <1 mg/kg to >100,000 mg/kg (10%) in lead ores. Averages in
the literature range from 10 mg/kg (Bowen 1966) to 37 mg/kg (Cholak e_t^ al.
1961) for uncontaminated soils (see Table 4-5). For an average of all
soils in the United States, Warren ^t al. (1971) estimated a lead content
of 20 mg/kg. DeTreville (1964) presents data indicating a concentration
of 16 mg/kg for the earth's crust, but with values as low as 0.04 mg/kg
in alluvial soil. In an estimate derived from surveys of the literature,
Nriagu (1978a) reported an average concentration of 18 mg/kg for the
United States. The natural sources that contribute to this background
level include weathering of rocks, volcanoes, and erosion of ore deposits.
Like lead in the atmosphere, the majority of anthropogenic lead in
the soil results from the deposition of lead emitted from the combustion
of leaded gasoline and, to a lesser degree, the emissions from industrial
4-10
-------
TABLE 4-5. CONCENTRATIONS OF LEAD IN SOIL
Description
Uncontaminated soil
Earth's crust
All U.S. soils
All U.S. soils
Chicago Expressway — <13.7miles
Chicago Expressway — 46 miles
Street dust
Dust — residential areas (IL)
Dust — commercial areas (IL)
U.S. city dust — residential
U.S. city dust — commercial
Urban soil — U.S. cities
Montana — 1 mile from smelter
Montana — 2 miles from smelter
Montana — 4 miles from smelter
Idaho smelter — .7-12 miles
Soil in vicinity of a barn
Soil in vicinity of a wooden house
Cincinnati house
Old house
Orchard soil — no pesticides
Orchard soil — pesticides with lead
Concen trat' on (m^/kg)
Mean Range
10-37
16
20
18
555
1636
2413
523
4000
600
100
2000
Minimum-.04
Max!mum-7600
Maximum-yOO
656-3067
1774-3549
99-834
300-7600
450-6338
32-7620
440-490
3-76
7-360
Reference
Bowen (1966), Cholak et ;il. (1961)
DeTreville (1964)
Warren vt al. (1971)
Nriagu (1978a)
Kahn et al. (1973)
Rameati (1973)
Schroeder (1974)
Schroeder (1974)
NAS (1972)
NAS (1972)
Chow et al. (1975)
U.S. EPA (1972)
U.S. EPA (1972)
U.S. EPA (1972)
Ragaini _et al. (1977)
Ter Haar and Aronow (1974)
Ter Haar and Aronow (1974)
Bertinson and Clark (1973)
Bogden and Louria (1975)
Chisolm and Bishop (1967)
Chisolm and Bishop (1967)
-------
activities, such as lead smelting. A 40-year study of soils in areas
of high traffic (Page and Ganje 1970) showed an increase in lead concen-
tration from 17 mg/kg to over 50 mg/kg in 1968. Kahn and co-workers
(1973) reported levels of lead in soil along a Chicago expressway as high
as 7600 mg/kg at distances <13.7 meters from the highway and 900 mg/kg
as far away as 46 meters. Before the use of automobiles, Nriagu (1978a)
theorizes that the primary source of lead contamination was flue dust
created by burning coal.
Lead in urban soils tends to be somewhat lower than that found in
the immediate vicinity of highways. In a sample of nine U.S. cities,
Chow _et al. (1975) reported soil levels in inner city parks ranged from
99 mg/kg in a Houston park to 834 mg/kg in New York's Central Park.
As a result of sampling 16 sites, the average concentration for these
cities was 523 mg/kg.
High levels of lead are also found in urban dust. Sartor and Boyd
(1972) found the following lead concentrations in dust from various
sites: industrial (840 mg/kg), residential (1100 mg/kg), and commercial
(1400 mg/kg). Rameau (1973) observed that the mean lead content of
street dust was 555 mg/kg,with 90% consisting of particles <250 y.
Although these are fairly wide ranges of concentrations, all city dust
contains relatively high levels of lead, with residential areas lower
than commercial areas. Schroeder (1974) reported 656-3067 mg/kg for
residential areas, and 1774-3549 mg/kg for commercial areas in nine
Illinois cities. Similar studies were conducted in several states.
With the exception of Virginia and Kentucky, the average level of con-
centration in commercial areas is almost double the residential level.
NAS (1972) compared 77 cities in the United States and found levels of
1636 mg/kg at residential sites compared with 2413 mg/kg at commercial
sites.
Although many authors have noted a decrease in the soil concentra-
tion of lead with increasing distances from the roadway (Nriagu 1978a),
lead concentration also appears to decrease with increasing depth in
soil. Numerous authors, including Tolonen (1974), Ward ^t. aj. (1975),
and Rolfe and Haney (1975), have reported that lead concentrations above
background levels are uncommon below a depth of 10 centimeters.
Although the effects of automobile exhaust have a wide national
impact, point source lead can produce extremely high local lead concen-
trations. Lead smelting operations probably have the most significant
impacts on nearby soils. In Helena, MT, the U.S. EPA (1972) reported
concentrations of 4000, 600, and 100 mg/kg of lead at distances of 1,
2, and 4 miles from a nearby smelter. Ragaini and co-workers (1977)
studied a lead mining and smelting operation near the town of Kellogg, ID,
where the majority of ambient lead originated in airborne emissions from
the complex. One of the highest concentrations in the soil, 7600 mg/kg,
was at the site closest to the complex, 0.7 mile, with other site
observations varying from a fairly high reading of 2200 mg/kg 12 miles
away to 300 mg/kg at a site 5 miles away. Unlike lead from automobile
4-12
-------
exhausts, the data show that smelter emissions affect areas up to
25 kilometers away (Bolter _e_t al. 1975, Koirtjohann _et al. 1975).
Soil samples in the vicinity of lead-painted houses have been found
to contain significant lead concentrations. Ter Haar and Aronow (1974)
reported soil levels ranging from 450-6338 mg/kg next to a wooden house
in Michigan and 2000 mg/kg near a Massachusetts barn. Bertinson and
Clark (1973) reported lead levels ranging from 32-7620 mg/kg in the
soil around a nineteenth century house in Cincinnati, and Bogden and
Louria (1975) found levels, averaging 175 mg/kg before and 440-490 mg/kg
after paint removal, in the soil surrounding an old lead-painted house.
Chisolm and Bishop (1967) have demonstrated the consequences of
using pesticides containing lead; lead levels of 7-360 mg/kg were found
in orchard soils compared with levels of 3-76 mg/kg in adjacent
nonorchard soils.
4.2.4 Biota
Numerous authors have shown that lead concentrations in biota
correlate with the concentration of lead in the surrounding environment.
Thus, background levels for biota are related to those previously
described for soil, water, and the atmosphere. In a study of pine
needles in North America, Elias and co-workers (1976) reported lead
concentrations of 10 yg/kg. It is believed that one-half of these
concentrations comes from natural sources. Smith (1973) reported that
grass growing in a relatively unpolluted environment contained lead
levels of -1-5 mg/kg. In an extensive study of naturally-occurring
levels of lead in bird tissues, Bagley and Locke (1967) found concen-
trations in the range of 0.5-3.7 mg/kg. Settle and Patterson (1980)
have estimated that natural lead levels in tuna, during prehistoric
times, was -.03 yg/kg. Studies of current effects of lead pollution
have shown concentrations of lead in the biota at over 900 times these
baseline levels (Settle and Patterson 1980).
A summary of selected levels of lead found in biota is contained
in Table 4-6. In general, elevated levels are found near highways and
point sources, such as smelters; in areas where lead-containing pesti-
cides have been used; and in terrestrial birds that have consumed lead
shot .
4.2.5 Limitations of Monitoring Data
In the evaluation of the monitoring data previously discussed, the
results of Settle and Patterson (1980) must also be considered. These
data show that background levels of lead, especially in tuna, have been
overestimated by as much as a factor of 1000. These authors suggest
that overestimates have occurred as a result of contamination in sample
collections and analyses. Thus, the data presented in the previous
4-13
-------
TABLE 4-6. CONCENTRATIONS OF LEAD IN BIOTA
Description
Vegetation
Background level - pine needles
Grass
Trees, shrubs, twigs -- Southeast
Leaves — Southeast
Salt marsh-cordgrass — MA
Marsh plants — dredge-spoil site
Leaf litter ~ MO (lead smelter)
Grass — ID (smelter)
Vegetables -- MO (lead belt)
Vegetables — control counties
Vegetables — NJ (9 meters from road)
Vegetables — SJ (76 meters from road)
Terrestrial Aniaals
Insects — high traffic volume
Insects — low traffic volume
Insects — high traffic volume
Insects — low traffic volume
Earthworms — 3-48 meters from road
Voles & mice — lead treated orchards (liver)
— untreated areas
Background level — birds
Duck wings
Woodcocks — U.S.
Aquatic Animals
Albacore, tuna, muscle (prehistoric period)
Albacore, tuna, muscle (present day)
Gastropods — CA
Mo Husks — CA
Oysters — East Coast
New tailings ponds — MO (crayfish)
New tailings ponds — MO (snails)
Fish — NY (lakes and streams)
Trout — Cayuga Lake
River fish - MT
Concentration (mg/kg)
Mean
0.01
154
70
6.2
17
3.8
8.6
1.7
23.4
-4
12.63
0.00003
0.0003
Ranee
1-5
<10-3000
< 10-2000
5.4-23.2
4,379-39,636
320-10,000
8.8-114
< 5-20.6
18-1742
8-212
Reference
52.7-270
0.5-3.7
0.5-361
4.51-29.79
.3-1.5
3.85
2.6-11.8
2.2-931
0.67-0.88
28-69
39-116
Max. 3
0.004-0.02
Elias _ejt al. (1976)
Smith (1973)
Connor and Shacklette (1975)
Connor and Shacklette (1975)
Banus £t al. (1974)
Drifmeyer and Odum (1975)
Gale and Wixson (1979)
Ragaini et_ al. (1977)
Hemphill zt_ al. (1971)
Hemphill £t al. (1971)
Motto ejc al. (1970)
Motto e£ al. (1970)
Price et al. (1974)
Price et al. (1974)
Giles et al. (1973)
Giles et al. (1973)
Gish and Christensen (1973)
Elfving et al. (1978)
Bagley and Locke (1967)
U.S. DI (1979)
Scanlon sit al. (1978)
Settle and Patterson (1980)
Settle and Patterson (1980)
Schwimer (1973)
Graham (1972)
Kopfler and Mayer (1973)
Gale et al. (1973)
Gale et al. (1973)
Pakkala e£ al. (1972)
Tong et al. (1974)
Pagenkopf and Neuman (1974)
4-14
-------
sections, related to background or control values, should be viewed
with caution.
4.3 Fate of Lead in the Environment
4.3.1 Introduction
This discussion on the fate of lead in the environment is based on
the results of discharges from processes that have been identified as
significant contributors of lead to the environment (see Chapter 3.0).
Emphasis is on the form of lead and its subsequent transport when
released to the environment. Versar, Inc. (1979) has conducted a general
overview of the environmental chemistry of lead, which has been used
in the formulation of judgments concerning the direction and rate of
transport lead assumes in an ecosystem. The literature available also
supports these observations.
The major pathways of physical transport and qualitative rates of
transport are designated in Figure 4-2. Atmospheric emissions (Pathway --1)
include point sources, such as lead production, incineration, smelting,
and coal combustion, that contribute to localized pollution; and dispersive
sources, such as automobile exhausts, that contribute to the concentra-
tions of lead found in urban air, urban dirt and dust, and urban runoff.
Pathway #2 follows the flow of lead that originates from solid waste
disposal areas and mine tailings. Because environmental controls may
restrain further discharges to air and water, the quantity of lead dis-
posed to land surfaces can be expected to increase. Lead discharges
contained within industrial process effluents into local surface waters
is reviewed in Pathway #3. The fate of lead in POTWs is described in
Pathway ??4.
A more general overview of all major pathways of anthropogenic
sources of lead is shown in Figure 4-3. The major effect on the air
compartment, which is the migration of groundwaters containing lead to
nearby surface waters, has not been shown in this figure because:
(1) the process is extremely slow, and (2) the current magnitude of this
transport pathway is not sufficiently documented. In addition, the high
concentration of lead in sediments with respect to the overlying water
and the steep profile of lead concentrations in soils subject to con-
tamination is not represented in this figure.
The following discussion is divided into two major sections:
(1) 4.3.2, General Fate Processes, which discusses the fate of lead in
its various forms when it reaches the air, water, or soil; and
(2) 4.3.3, Major Environmental Pathways, which discusses the fate of
lead as a result of specific sources.
4.3.2 General Fate Processes
4.3.2.1 Atmospheric Transport
The atmospheric transport of lead depends on particle size, the
height of the release, geographical distribution, and the chemical form
4-15
-------
Pathway No.
1.
I
M
O\
Atmospheric Emissions
Pb Production
Iron and Steel Production
Fossil Fuel Combustion
Zinc and Copper Smelting
Iron and Steel Production
Automobile Emissions
Solder Use
Local
Soil Surfaces
Solid Waste and Tailings
Primary Pb Production
Ammunition
Solder Use
House Paint
Weights and Ballast
Bearing Metals
Iron and Steel Production
Copper and Zinc Smelting
Dissolved Solids
Susp. Sediment
FIGURE 4-2 MAJOR ENVIRONMENTAL PATHWAYS OF LEAD EMISSIONS
-------
Aqueous Discharges _
Treatment System
Iron and Steel Production
Lead Production
Coal Mining
Pulp and Paper Industries
Nnnfprrnii<; Mptalc
^-
i
Effluent
\)
Hazardous/Solid
Waste Dump
X
m
POTW
Pathway # 4
' Surface Water (
1 Sediments
Slow
—
Ground Water
^ Oceans
S
<&
-C-
I
1
POTW Primary
Influent Treatment
\
^_
\,
Biological
Treatment
*
Sludge
Effluent
Ocean Dumping
Incin-
eration
lan.llill
1 ^~
Air
Soil
»•-
Slow
|
Surface Waters '
Sediments '
>
t.
Ground Water
S
^
FIGURE 4-2 MAJOR ENVIRONMENTAL PATHWAYS OF LEAD EMISSIONS (Continued)
-------
Automobile
Emissions
of Lead
Washout
Dry Fallout ^yv
to Water N/S.
Washout and
Dry Fallout
to Land
Oceans and
Ocean Sediments
Surface Waters
•M
[POTW
Other Anthropogenic
Sources of Lead
Land
Surface Soils
Tailing Piles
Landfills, etc.
Note: Quantities of lead moving in each pathway are roughly proportional
to the thickness of each pathway shown. Slow movement from
ground waters to surface waters is not shown.
FIGURE 4-3 SCHEMATIC DIAGRAM OF MAJOR PATHWAYS OF ANTHROPOGENIC SOURCES OF
LEAD RELEASED TO THE ENVIRONMENT IN THE UNITED STATES, 1976
4-18
-------
of lead emitted. Although all these processes are significant, the
chemical form probably has the least effect on transport and deposition.
Larger particles, particularly >20 ym in aerodynamic diameter, are
rapidly deposited. Atmospheric turbulence predominantly controls the
deposition of particles <20 ym, by "forcing" the particles to the surface
where they are deposited by impaction. Atmospheric parameters control
the deposition velocity for particles <20 Mm (deposition flux/air con-
centration), which is relatively independent of particle size and ranges
from 0.1 to 10 cm/sec. The deposition velocity for a 20-Mm particle
ranges from 2 to 10 cm/sec, while particles >50 ym settle at velocities
>10 cm/sec (Sehmel and Hodgson 1976).
The initial height of release is another significant factor in the
determination of the distribution of airborne lead and its deposition
patterns. Particles released near ground level are more likely to
contribute to high ground level concentrations, x^hich lead to human
exposure, and are more likely to be deposited by impaction, which leads
to deposition patterns that decay rapidly with distance from the source,
such as those observed near highways and ore mines. It is much less
likely that turbulent processes will bring particles released from
elevated sources (particularly with diameters <20 ym) to ground level;
thus, they will be dispersed over greater distances and will most likely
be brought to the ground by precipitation with more widespread impacts.
This is to be expected for smelter and coal emissions.
The geographical distribution further distinguishes the major
source type. Although a considerably smaller source than automotive
emissions on the national scale, ore mining, milling, and smeltering are
concentrated in a few isolated major sources. This has led to acute
localized impacts on isolated ecosystems. Automotive emissions distri-
buted along every major thoroughfare may lead to lower resultant concen-
trations but a much greater risk of exposure to lead.
Finally, the chemical form of emitted particulates can affect
deposition; lead sulfates and nitrates tend to be hygroscopic and may
preferentially be rained out by in-cloud scavenging processes. Other-
wise, the chemical form of a particulate is unlikely to affect its
atmospheric transport and deposition.
4.3.2.2 Fate Processes in Aquatic Environments
Because the aqueous environmental chemistry of lead has been
extensively discussed by Rickard and Nriagu (1978), only a brief
discussion will be contained here. •
Aqueous Complexation
The concentration of soluble lead in water is directly related to
parameters, such as pH, the oxidizing potential of the water (indicated
as pE), the presence of competing ions (Ca^, Mg4^, Fe"^), and the
existence of precipitating and complexing agents. According to the
4-19
-------
model calculation of Vuceta and Morgan (1978), who used input parameters
that simulated an aerated freshwater system, Pb(II) is present as the
free metal ion below pH 7.1 and complexed with carbonate ion above that
pH. Adsorption and complexation with hydroxide ions account for the
remaining lead in the water column. Lead is strongly complexed by organic
acids, such as huraic and fulvic acids (Rickard and Nriagu 1978). Again,
pH controls the equilibrium of complexation: at pH 3.5, the log of"the*
equilibrium constant (log K) is 3.09, while at pH 5 the tendency to com-
plex with fulvic acids increases as indicated by a log K of 6.13. At
this pH, lead is exceeded only by copper in its ability to complex with
organic acids. In interstitial waters, ^80% of the total lead may be
found complexed to organic molecules (Rickard and Nriagu 1978).
Sediment Adsorption
In natural freshwater systems, lead will be sorbed onto clay prefer-
entially over calcium and potassium ions, with the tendency for sorption
decreasing in the following order: kaolinite >illite >montmorillonite
(Nriagu 1978a). Various parameters, such as surface area and the crystal
type, dictate the adsorption of lead onto hydrous iron and manganese
oxides. Although hydrous iron and manganese oxides exert less control
over lead than clays and organic matter, lead is strongly adsorbed in
comparison with other trace metals. Figure 4-4 indicates that lead is
exceeded only by copper in its ability to be sorbed by silica and hydrous
oxides (Vuceta and Morgan 1978). Adsorption to these surfaces is essen-
tially irreversible; Rickard- and Nriagu (1978) suggest the following
mechanism:
i /^
Pb + Mn02 + H20 ^PbMnO (OH) + H+
(quenselite)
Pb+2 + Fe(OH)3 »-PbFeO(OH)2 + H+
(amorphous)
Serne (1977) conducted several extraction techniques on the sedi-
ments of the San Francisco Bay. His results indicated that 45% of the
lead was associated with organic matter and sulfides; 50% of the lead
was inert to chemical attack, within clay lattices; the remaining 5% of
the lead in the sediments was associated with iron and manganese oxides.
Transport of Lead in the Water Column
Perhac (1974) studied three streams in Tennessee to ascertain the
nature of trace metal transportation. He found that lead was highly
concentrated in suspended solids. Because the suspended solids were
such a small percentage of the total solids in the water column, however,
the bulk of the lead was transported in the dissolved state. Table 4-7
is a summary of these findings.
4-20
-------
10
Note: (pH = 7, pE = 12, pC02 = 10"8-5 atm., pCt-4.16)
as a function of surface area of SiC^ in ha/?.
pS = -log(Si02)ha/£.
Source: Vuceta and Morgan (1978).
FIGURE 4-4 ADSORPTION OF HEAVY METALS IN
OXIDIZING FRESH WATERS
4-21
-------
TABLE 4-7. CONCENTRATION AND DISTRIBUTION
OF LEAD IN THE WATER COLUMN
Concentration % of Mass in the % of Pb in
Pb (mg/kg)
Water column
Dissolved solids
Colloidal solids
Coarse particulates
Sediments
these numbers are averages of 6 sites, and thus do not add to 100%.
Source: Perhac (1974).
0.015
83
1683
278
74.5
•--— — — — W.A. u*t*«* * * t*L U- ^ J. \jWiUlUH
94.6 90.8
0.17 1.2
8.96 8.0
—
4-22
-------
Aquatic Biological Pathways
Natural levels of lead are commonly found in freshwater ecosystems
and less commonly in marine systems. The metal does not appear to be an
essential nutrient; however, it is present at background levels in
organisms living in relatively nonpolluted areas. Most studies report
tissue concentrations of lead measured in the environment without the
specifications of the water concentrations that lead to these levels.
These are described in Section 4.2. The subject of lead bioaccumulation
has been discussed in detail by Bell et al. (1978), Phillips and Russo
(1978), and Wong _et .al. (1978). The mechanism of bioaccumulation and
the parameters that influence it are described briefly in the following
section.
Parameters Affecting Uptake
The potential routes for exposure to and uptake of lead by aquatic
organisms are ingestion and absorption across the derma and respiratory
organs. For invertebrate filter-feeders, ingestion of suspended parti-
culate matter that contain adsorbed or complexed lead is an important
route (Armstrong and Atkins 1950). For higher trophic level species,
ingestion of detritus vegetation and other animals contaminated with
lead is an important route (Bowen and Sutton 1951). Because of the
high lead concentrations associated with fish, for them, ingestion of
crustaceans may be an important source (Hardisty et al. 1974). Several
physiological processes may be involved in complexation of the lead with
organic molecules (Schubert 1954), incorporation of lead ions (Williams
1953, Lehninger 1970), and uptake by exchange (Korninga 1952).
Several parameters, both biological and environmental, influence
bioaccumulation of lead. Even under uniform exposure conditions,
variability between species is important (Wong et al. 1978); however,
more controlled assays are needed to determine its significance. In
certain fish, bioaccumulation decreases with age, although it may be a
result of the consumption of a lower fraction of zooplankton by younger
fish (Schell jet al. 1974). The calcium status of the exposed indivi-
dual also influences uptake and retention of lead, which is reduced with
increased Ca availability (Varanasi and Gmur 1978). In estuarine fish,
the lead concentration in water, duration of exposure, temperature, and
water salinity affect bioaccumulation (Sommers et_ al. 1976).
Bioconcentration Factors (BCF) and Biological Half-lives
Lead bioaccumulation levels and bioconcentration factors (concen-
tration in tissue/concentration in medium) are presented in Table 4-8
for a variety of fresh and marine aquatic species, both invertebrates
and vertebrates. The studies were conducted under a wide range of
conditions and are not strictly comparable. Most organisms were exposed
to lead dissolved in water; however, a few studies exposed species to
suspended particulate lead or to contaminated sediment. In some cases,
lead concentrations were measured in specific organs rather than in the
4-23
-------
TABLE 4-8. LEAD BIOACCUMULATION LEVELS AND BIOCONCENTRATION
FACTORS IN AQUATIC SPECIES
Species
Oysters (Crassostrea
Virginia)
it
Freshwater Clams
(6spp. )
Freshwater Clams
(8 spp.)
Mussel (Mytillus
galloprovincialis)
6 Invertebrate
Species
Brook Trout
(Salvelinus fontinalis)
Brook Trout
Brook Trout
Coho Salmon
(Oncorhynchus kisutch)
Coho Salmon
(Oncorhynchus kisutch)
Fish (Gillichthys
mir ab ilis)
Water Con-
centration
(ug/1)
0.5-3.0
(Mobile, AL)
25-200
5.2-89.6
g/g (sedi-
ment) 0.021
(water)
(sediment in
Mississippi)
0.29-2.15 ng/g
particulate
lead suspended
in water
32.0-565.0
119.0
3.0
12.0
0.21
lab
150
38
Tissue Con-
centration BCF
(mg/kg) (Approximate)
0.67-0.88a 200-1760
9-1153 4600
(muscle)
28-368 147203
(liver)
up to 48b
(body)
lla
3.9-9.5b 4400-13400
up to 500b 1000-9000
68b (liver) 570
215b (kidney) 1800
4.2b (liver) 1400
56. Ob (liver) 4600
1.4b (muscle) 100
68b 300
(gills)
50 (kidney) 200
10b (liver) 50
1.5 (gills) 10
0.4 (liver) 4
22b (gills) 580
Reference
Kopfler and Maver
(1973)
Pringle at al.
(196S)
Anderson (1978)
Price and Knight
(1978)
Marietta et al.
(1979)
Spehar et al .
(1978) ~~
Holcombe et al.
(1976) ~
Pagenkopf and
Neuman (1974)
Ray (1978)
Varanasi and Gmur
(1978)
Reichert et al .
(1979)
Stenner and Nickless"
(1975)
Wet weight.
Dry weight.
£
All values were calculated from given water concentration and tissue levels.
Otherwise factor is as reported by the authors.
Pteronarcys dorsata. Hydropsyche betteni. Brachycentrus sp., Ephemerella sp.
Physa integra and Gammarus pseudolimnaeus.
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total body. Tissue levels generally ranged from two to four orders of
magnitude above water concentrations.
Preferential accumulation of lead in certain organs has been
reported in various studies. In fish, the liver and kidney usually
have higher concentrations than muscle and gill tissue (Leland _et al.
1979, Ray 1978, Hardisty et al. 1974). The digestive tract sometimes
contains high lead levels (Adams 1975), which implicates diet as an
exposure route (Bryan and Uysal 1978). In mollusks, the muscle frequently
contains high lead concentrations (Pringle et al. 1968, Gire _et al. 1974).
Limited information on biological half-lives indicates that lead is
retained in tissue for at least several months (Schulz-Baldes 1974).
Half-lives for invertebrate species of 300 days in the soft parts of
Mytilus edulis. 170 days in Mesidotal entoman and 50 days in Harmatoe
were reported (Kauranen and Jarvenpaa 1972). Reickert and co-workers
(1979) observed no increase of lead concentrations in the kidney or liver
of the coho salmon during a five-week exposure to clean water following
a two-week exposure to lead. A depuration rate of 0.48-0.91 mg/kg/day,
however, was measured in the eastern oyster (Pringle ejt al. 1968),
which indicates the presence of an effective excretion mechanism for
eliminating the metal.
Tetraalkyllead compounds have been detected in fish tissue from
various locations (Mor and Beccaria 1977, Harrison 1977, Chau .et al.
1979). Rainbow trout bioaccumulate tetramethyllead as much as three
orders of magnitude above water concentrations of the compound (Chau et al.
1979). No direct sources of tetramethyllead to the environment are knownT
however, certain sediment microorganisms are capable of methylating
inorganic lead nitrate or trimethyllead acetate to tetramethyllead, a
more mobile and biologically accessible form of lead (Summers and Silver
1978). It is unknown how significant this process is in aquatic sediments
or its influence on biotic uptake. Most of the lead in anaerobic sediment
is expected to be immobilized as lead sulfide in the presence of sulfur
(Rickard and Nriagu 1978); therefore, it is generally unavailable for
release into the water column.
Biomagnification in Food Chains
It does not appear that lead concentrations in aquatic biota increase
at higher trophic levels (Anderson et al. 1978, Drifmeyer and Odum 1975,
Namminga et al. 1974, Mathis and Cummings 1973); rather, the exposure
pathway is a more important factor in lead bioaccumulation, as described
previously. In fact, secondary consumers often have lower concentrations
of lead than lower food chain members (Wong jt_al. 1978). Phytoplankton
and zooplankton have been reported to have high lead concentrations in
comparison with other species in the same ecosystem (Namminga et al.
1974). Herbivores and detritivores are likely to accumulate higher
concentrations than carnivores (Leland and McNurney 1974). An explana-
tion for preferential uptake by these organisms is the strong association
of lead with sediment and organic matter and low levels in the water
column.
4-25
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4-3.2.3 Fate Processes in Terrestrial Environments
Movement in Soil
Lead is found in the following ores: galena (PbS), plattnerite
(Pb02), cerussite (PbC03), and anglesite (PbS04). The earth's crust
averages approximately 15 yg/g of lead. The chemistry of lead in soils
is dominated fay adsorption and precipitation reactions, which are
functions of the soil texture, cation exchange capacity (CEC), pH and
in part, phosphorous content (P).
Several researchers have proposed regression equations to determine
the quantity of lead sorbed per gram of soil. For instance, the quantity
of lead sorbed as a function of the above mentioned parameters is
determined by the following equation (with a correlation coefficient
of 0.997):
Pb = 34.3 + 0.0774P + 5.358 pH + 5.337 CEC
where Pb is in ymoles/g soil (Zimdahl and Hassett 1977).
As indicated in Figure 4-5, lead is adsorbed quite strongly by
soils, exceeded only by copper. The lead ion is adsorbed above PH 5
Below this pH level, precipitation as PbQ and organometallic completion
are the control mechanisms of Pb in solution (Zimdahl and Hassett 1977)
Lead has a strong tendency to sorb onto soil particulates as indicated
from the results of most soil column leaching studies. A literature
review by Zimdahl and Hassett (1977) revealed one study in which only
17 yg/g soluble Pb was present in the soil solution three days after
application of 2784 ug/g PbNO The remaining lead had been sorbed.
Another study applied the equivalent of seven years rainfall to a soil
column containing 460 yg/g Pb. Only 1.6% of the applied Pb was leachable.
Jennett et al. (1977) also found that neutral water was not capable of
desorbing lead, or causing Pbs to come into solution. A recent study
Stevenson and Welch (1979), determined the extent of downward migration
that occurred within 6.5 years of lead applications ranging from 0 to 3200
kg/ha Pb. Although Figure 4-6 illustrates that the increased levels of
Pb can be observed to a depth of about 60 centimeters, the initial lead
had been applied to a depth of 15-30 centimeters. Below a 60-centimeter
depth, the values approached background levels.
Because lead is readily sorbed onto soil particles, the movement of
lead with runoff is likely. Entrainment of soil particles is also a
possible route of lead transport.
Terrestrial Biological Pathways
Parameters Affecting Uptake
Plants are exposed to lead by aerial deposition on leaves, stems,
or bark, and by root uptake from the soil. Aerosol lead can accumulate
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200
.2
o
£
e
c
100 -
2345678 9 10
PH
Source: Huang _etaL (1977).
FIGURE 4-5 ADSORPTION OF HEAVY METALS ON
SOIL MINERALS AND OXIDES
4-27
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0-15
15-30
5 30-45
E
a.
3J
Q
45-60
60-75
75-90
0 kg/ha/ 800 kg/ha
1600 kg/ha
3200 kg/ha
1.0
Source: Stevenson and Welch (1979).
2.0
log [Pb] mg/fi
3.0
4.0
FIGURE 4-6 DOWNWARD MOVEMENT OF LEAD IN SOIL
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in particulate form on plant foliage. Although there is controversy
concerning the extent to which plants can accumulate lead from aerosols,
it is generally thought to be minimal (Bell et al. 1978), primarily
because of the insolubility of lead (U.S. EPA 1977). It is difficult to
obtain data on plant accumulation of lead because of the problems associ-
ated with the differentiation between lead deposited on and lead absorbed
by the foliar tissue (Bell _et_ al. 1978). Studies of plant uptake near
automobile exhaust indicate that leaves have an extremely small like-
lihood of absorbing both the soluble and particulate forms of lead
(Koeppe 1977). The amount of lead that can be washed from leaves has
been reported to be 50% with a range of 8-80%. The amount removed
depends on the leaf surface; lead retention is higher in plants with a
rough or hairy surface (Peterson 1978).
Rooted plants are not considered good sensors of airborne lead levels
and attention is being given to the use of bryophytes. Little and Martin
(1972) reported that elm and hawthorne leaves could only retain 17% of
the total aerial lead fallout. They indicated that 30-90% of the fallout
on the foliage usually exists as a superficial coating that can be easily
washed off by rain, wind, etc. (Rickard and Nriagu 1978).
The soil environment is an important influence on the amount of
lead accumulated. The soil factors that can result in a maximum binding
of lead, and thus a reduced plant uptake, include a high cation exchange
capacity, pH, organic matter content, and phosphorous. Other factors
that influence uptake are soil temperature, calcium availability, soluble
silicon, soil texture, and the geological background of the soil. Zimdahl
and Koeppe (1977) found that the concentration of lead in oats and alfalfa
increased with a decrease in pH and organic matter, and that the addition
of phosphorous reduced the uptake of lead. However, the association of
lead and organic matter has not always appeared consistent (U.S. EPA 1977a)
Still, it is difficult to determine the actual amount of lead taken
up by plant roots because much of the lead is bound on the plant surface
as crystalline or amorphous deposits. Appreciable uptake of lead occurs
from hydroponic solutions, which do not have complicated binding para-
meters (Koeppe 1977). Warren (1978) concluded that no simple relation-
ship exists between the lead content of vegetables and the soil in which
they are grown and that each vegetable has a characteristic lead accumula-
tion ability. In general, the overall mean plant/soil ratio of lead was
8%. However, not all vegetables growing in lead-contaminated soil will
exhibit elevated levels of lead (Peterson 1978).
The amount of lead absorbed by vegetation and moved into above-ground
portxons depends on the species, soil type, and many environmental factors.
4-29
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The amount translocated is generally low. The highest lead concentra-
tions are usually associated with the organ that has the greatest surface
to volume ratio and the roughest or most pubescent surface, generally the
roots (Peterson 1978, Smith 1976). In general, there appears to be a
7- to 10-fold decrease in lead concentration from root to foliage and a
similar decrease from foliage to grain (Zimdahl and Koeppe 1977).
Bioconcentration Factors
A few bioconcentration factors (BCF) for different species of vege-
tation are calculated in Table 4-9. The high degree of variability
reflects species differences as well as differences in exposure sources.
Yopee and co-workers (1974) have recommended that the maximum permissible
level of lead to which crop plants are exposed should not be >2.0 mg/kg
when soluble in soil solution.
Numerous studies have investigated lead bioaccumulation in terres-
trial invertebrates, such as earthworms (Gish and Christensen 1973,
Gullvag 1978) and grasshoppers (Scanlon 1978), and in vertebrates, such
as small mammals and birds (Clark 1979, Roberts et_ al. 1978, Haschek
_et al. 1979). Some of the measured tissue concentrations are reported
in Section 4.2, Distribution of Lead in the Environment. Unfortunately,
it is very difficult to relate environmental media concentrations to the
extent of lead uptake in terrestrial animals because of the many exposure
pathways possible (e.g., ingestion of contaminated food, inhalation,
dermal absorption from soil, etc.)- No laboratory studies were found
that might have provided insight into exposure levels and bioaccumulation
in terrestrial animals.
4.3.3 Major Environmental Pathways
4.3.3.1 Pathway #1 — Atmospheric Transport
Atmospheric
Emissions
Groundwater
Ocean
POTW
Air
•Pathway #4
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TABLE 4-9. LEAD ACCUMULATION BY VEGETATION
Species
Field Studies
Oak roots
.4 km away
2.0 km away
control
Mixed Species
Fall
Spring
Fall
Spring
Lettuce
Potato
Source
Lead smelter
Lead smelter
Lead smelter
Control
Control
Highway
47,100 car/
24 hrs
30 ft from
road
Highway
47,100 car/
24 hrs
30 ft from
road
Exposure
(mg/kg)
Soil: 6376
Soil: 208
Soil: 140-190
Soil: 13.6-25
Soil: 52
dry wt
Soil: 88.6
Soil: 13
Soil: 18.9
Air: 4. 5 Ug/m^
Soil: 134
Air: 4. 4 wg/m3
Soil: 134
Accumulated
(mg/kg)
2400
6.0
3.0
Roots: 208
Unwashed
Tops: 326
Roots: 309
Unwashed
Tops: 823
Roots: 12.7
Tops: 25.8
Roots: 22.3
Tops: 37.6
Leaves: 24
Roots: 24
Leaves: 87
Roots: 33
Calculated BCF
.36
.02
.08
.08
Roots: 4
Roots: 3.49
Roots: .98
Roots: 1.18
Whole plant:
48/138.5=
.35
Whole plant:
120/138.5=
.87
Reference
Jackson and
Watson (1977)
Peterson (1978)
Peterson (1978)
Peterson (1978)
Peterson (1978)
Bell et al.
(1978)
Bell et al.
(1978"5
Laboratory Studies
Barley
Apple leaves
Corn tops
Laboratory
Potted soil &
colored news-
print
4 weeks in lab
soil without
optimum pH,
CEC & phos-
phorous for
binding pH
Hydrophonic
for 3 days-
Soil: 800
567 (dry)
(2nd yr)
2000 soil
Roots: 800
dry wt
Tops: 3
dry wt
Roots: 1.0 Zimdahl and
Koeppe (1977)
7.71 dry wt 0.01
(5.50 control)
200-400
dry wt
0.1-0.2
Elfving et al.
(1979)
Koeppe (1977)
100 ug Pb/ml Roots:10,600 Roots:106
dry wt
Tops: 390 Tops: 3.9
dry wt
Koeppe (1977)
4-31
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Sources
Pathway #1 describes the fate of lead entering the atmosphere
as a result of the combustion of gasoline with lead alkyl additives;
the storage and distribution of leaded gasoline; mining, milling,
and smelting of primary lead ores; zinc and copper smelting; fossil
fuel combustion; and iron and steel production. Each of these sources
is unique with respect to the chemical and physical form of the
emitted lead and the geographical and vertical source distribution.
Except for the evaporation of tetraethyl and tetramethyl lead from
leaded gasoline, most atmospheric emissions of lead are in the particu-
late form.
Automotive Emissions — Antiknock Additives
The lead alkyl gasoline additives, tetraethyllead (TEL) and tetra-
methyllead (TML), may be released by evaporation during storage or
distribution. The release of these additives appears to be the predom-
inant mechanism rather than combustion, since the highest concentrations
of organoleads have been reported in samples taken near a busy gas
station (0.59 yg/m3) and in an underground'parking garage (1.8-2.2 yg/m3)
(U.S. EPA 1977a). Organolead concentrations comprised 10 and 17%,
respectively, of the total airborne lead. Laveskog (1971) also observed
small amounts of vapor phase tetraalkyllead compounds in automobile
exhaust, where they are likely to be quickly adsorbed onto exhaust
particulates (Harrison and Laxen 1978). In urban air, organoleads
typically comprise 1-4% of the total airborne lead (Harrison and Perry
1977).
Harrison and Laxen (1978) recently investigated the chemistry of
TEL and TML in ambient air. They concluded that like the atmospheric
chemistry of other hydrocarbons, homogeneous gas phase reactions predom-
inate in the breakdown of these compounds. Their results indicate that
daytime decay rates for TML range from 3-29%/hr, and for TEL, 17-93%/hr.
The stable lead compounds formed by these decay processes have not been
identified.
Automobile Exhaust
The U.S. EPA (1977a) has effectively summarized data on the
particulate sizes associated with exhaust from leaded gasoline combustion
in automobiles. Under cruise conditions, automobile exhaust contains
lead in extremely small aerosol sizes. The reported mass median diameter
is generally 0.5-pm or less. Chamberlain et. al^. (1975) report even
smaller sizes (0.015 ym). Particles <0.1 ym rapidly coagulate via
Brownian motion to form particles 0.1-0.5 ym in diameter. On the other
hand, during cold start or acceleration, the particle sizes are consi-
derably larger, with mass median diameters in the range of 2-10 ym.
Haibibi (1973) and Ter Haar et al. (1972) found that the mass median
diameter increased with vehicle mileage. Ter Haar and co-workers (1972)
estimated that approximately 35% of the Pb burned over the lifetime of
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a car is emitted as fine particulate (<0.5 m) and 40% is emitted as
participates (>0.5 m) . Thus, actually only 75% of the lead burned is
released to the atmosphere.
The predominant chemical form of lead in automobile exhaust is
PbBrCl. During acceleration, with hotter exhaust conditions, the
PbBrCl deposited in the exhaust system is released either by scouring
or vaporization.
Biggens and Harrison (1980) hypothesize that the reaction of
PbBrCl leads to the release of HBr and HC1 in acid sulfate droplets
(H2SC>4 and NH^SO^). This mechanism may account for the observed
decrease in Br/Pb ratios in aged urban aerosols, and may produce rela-
tively insoluble PbSC>4, which is a significant component of urban lead
aerosols that has been shown to increase in concentration in aged
exhaust aerosols (Ter Haar and Bayard 1971) and road dusts (Biggins and
Harrison 1980, Olson and Skogerboe 1975).
In rural environments affected by automotive exhaust, but presumably
exposed to lower concentrations of S02, sulfates, and photochemical pre-
cursors, Ter Haar and Bayard (1971) observed that the predominant lead
compounds were PbBrCl, PbC03, PbOx, and (PbO)2PbC03, with lesser contri-
butions from PbCl£ and
Wet/Dry Deposition
Automobile exhaust is emitted very close to the roadway, which is
an important factor in the substantial dry deposition near the roadway.
Large particles (> 20 ym) are expected to be deposited on the roadway
or within a few meters. Smaller particulates will also experience large
deposition rates by.impaction near the roadway as a result of their high
groundlevel concentrations. Nonetheless, a significant fraction,
probably on the order of 20-50% of the emitted lead, is associated with
fine particulates that are carried as aerosols away from the source and
comprise the bulk of the urban lead aerosol observed at greater distances
(< 100 meters) from heavily travelled roads (U.S. EPA 1977a).
The significant fraction (probably 20-50%) of automotive lead that
is transported from the immediate source is expected to be deposited,
possibly at great distances from the source, by precipitation. The
long-term impacts may be significant, particularly in mountainous regions
that receive large rainfall. These areas scavenge effectively both water
and lead from the air.
In the northeast, this rain is likely to be acidic (ph <5.6), which
would enhance the solubility of Pb by exacerbating the impacts on surface
waters. For example, Hirao and Patterson (1974) found that nearly all
of the lead entering an isolated High Sierra mountain watershed was of
anthropogenic origin, which was dominated by emissions from combustion
of leaded gasoline. This lead was delivered to the watershed via snow-
fall (92%) and dry deposition on foliage (8%). Ninety-eight percent of
the lead entering the watershed each year is held there and is primarily
4-33
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associated with organic matter in the uppermost soil horizons. The
reported deposition rate (0.9 mg/m2/yr) is one of the lowest observed
worldwide (Nriagu 1978a). Thus, at great distances from sources of
automotive lead, wet deposition is the predominant air-to-surface
pathway.
This is not to suggest that washout of automotive lead near road-
ways is not important. Indeed, washout rates near roadways are much
greater than those observed in the High Sierra: Atkins & Kruger (1968)
observed wet deposition rates of 40 mg/m2/yr in Palo Alto. However,
washout was only 24% of the total deposition in Palo Alto.
Deposition on Soils
Once lead is deposited, it is held strongly in the soil,usually
in the upper 1-5 centimeters. The understanding of the chemical forms
and fate of lead in soils is limited because of insufficient analytical
data. Olson and Skogerboe (1975) found that 50-70% of the lead in
roadside soil samples existed as PbS04. Other compounds identified
included PbO-PbS04, lead oxides, metallic lead, and PbS. The conversion
of PbBrCl to PbS04 may occur either in the atmosphere prior to deposi-
tion, or in the soil. Biggins and Harrison (1980) essentially confirmed
these findings, identifying also PbS04-(NH4)2, Pb304, and 2PbC03-Pb(OH)7.
Elemental lead was associated with sites where vehicle cold-starts occur.
PbS04 is one of the more soluble of these compounds, although all are
relatively insoluble at typical soil pHs. Lead is generally associated
with organic matter in the soil (Siccama et al. 1980). All" studies find
that lead is strongly associated with the solid phase in the soil
environment.
This fact, combined with the observed concentration of lead in the
upper soil horizons, implies that erosion and washoff of soil particles
by surface runoff is the major pathway for surface water contamination by
lead deposited from the atmosphere. Bertine and Mendeck (1978) studied lake
sediments in the vicinity of New Haven, CT in order to examine contami-
nation of surface waters by lead in urban areas, where the primary lead
inputs are from automotive exhaust. In this particular watershed, lead
contamination from the late 1800s to 1920 was predominantly related to
coal consumption; after 1920, automotive lead was the predominant input.
KLeinsman and co-workers (1977) analyzed Pb fallout and runoff in New
York City and suggested that automotive sources contribute a major
fraction of the lead input to the New York harbor.
Dry deposition of lead may also occur on vegetative surfaces. The
lead on these surfaces is generally easily washed off; and it is unlikely
that significant plant uptake occurs.
Smelters, Coal and Oil Combustion and Iron and Steel Production
Lead emissions from coal and oil combustion, smelters, and iron
and steel production are similar in that most of these emissions are
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released from elevated point sources. In general, baghouses or electro-
static precipitators control participate emissions from smelters and
many fossil-fuel utilities. These precipitators release only the smaller
particulates. Furthermore, because of the condensation process that forms
lead particulates at high temperatures, lead tends to be concentrated in
the finer particulates, which are generally <1 ym. Consequently, these
particulates are widely dispersed and are deposited predominantly by
precipitation.
The chemical characterization of these sources are expected to
differ, although the precise chemical characterization of lead contain-
ing aerosols from these sources is unknown. Corrin and Natusch (1977)
cite unpublished studies that show PbS, PbS04, and elemental lead as
the predominant lead species in smelter baghouse exhaust. Nriagu (1978b)
indicates all of the above lead species, plus PbCC^, PbO'PbS04,
PbO-PbS04, Pb included in other metal oxides, and lead silicates as
possible chemical forms in smelter exhaust.
Apparently, lead in particulates is preferentially adsorbed onto
the surface of the smaller silicate particles or included in soot
particles (Corrin and Natusch 1977). Nriagu (1978b) also suggests the
presence of PbOx, PbS04, Pb(N03)2, and PbO-PbS04.
Lead from smelters or fossil-fired utilities is likely to be quite
insoluble, although the lead sulfates, which may be a major component
of smelter exhaust, are relatively more soluble than the other forms.
Deposition on Soils
The effects of smelter emissions have been intensively studied.
Jennett et al. (1977) performed a study of a forest ecosystem contami-
nated by lead emissions in the New Lead Belt of southeastern Missouri.
Smelter emissions were found to result in significant deposition of lead
at least as far as two miles from the smelter. Basically, fugitive dusts
generated during ore transport and handling are the predominant cause
of extremely high deposition rates within 1000 feet of the smelter.
Almost one-half the particulate lead in the smelter stack emissions is
associated with particles <1 ym diameter. On the other hand, fugitive
dusts show a mass median diameter of about 7 ym, with 40% >10 ym.
Deposited lead is concentrated in the upper one inch of the soil
profile where the surface is covered by leaf litter. In locations
without surface leaf litter, several inches of the soil profile were
contaminated. Exposed plant parts (grasses, tree leaves, lettuce, etc.)
are seriously contaminated by lead, while roots and tissues are relatively
uncontaminated. This tendency of lead to be associated with surface
vegetation and leaf litter (as observed in roadside environments) causes
contamination of surface waters by runoff and soil erosion. In storm-
water analyses, Jennett and co-workers (1977) demonstrated surface water
contamination by showing relatively constant low levels of dissolved
lead throughout two storms, while levels of suspended lead increased
4-35
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dramatically in phase with stonnwater flow and suspended solids content.
These sediments are subsequently deposited in man-made lakes, which
drain the contaminated watershed (Jennett _e_t al. 1977).
The Walker Branch watershed of Oak Ridge, TN is predominantly
affected by coal-fired power plants. Studies by Andren _et al. (1975)
are apparently the only observations of lead deposition that focus on
coal-derived lead. The observed deposition rates of 60 mg/ta2/yr are
typical of those reported universally and summarized by Nriagu (1978b).
As expected for emissions from a coal-fired utility with tall stacks,
~67% of the lead deposition was by wet deposition.
Mining and Milling of Lead Ores
Mining and milling of lead ores create fugitive dusts comprised
primarily of PbS, but also containing PbC03, PbS04 Pb5(P04)3Cl, lead
oxides, and lead silicates. The particle sizes are large and the sources
are at ground level. Under these conditions, one would expect extremely
localized concentrations and depositions, based on Jennett and co-workers'
(1977) observations in the vicinity of mines, mills, and on haul roads.
The PbS particulates are insoluble and will be subject to runoff during
storms. Foraging species may become significantly contaminated (Jennett
et al. 1977).
Summary
The principle source of atmospheric lead emissions is from auto-
mobile use. The fate of lead depends on the size distribution of the
lead particulates, which, in turn, is a function of the operating condi-
tions of the car. Cold starts, and stop and go traffic, promote large
particle sizes and immediate deposition; cruise conditions form smaller
lead aerosols, which are subject to wider dispersion. The height of
lead release causes the greatest impact near the road. A significant
20-50% remains airborne, however. Lead emissions from mining and smelting
operations cause localized high concentrations of lead. Smelters and
other sources, which have higher stacks, allow for greater dispersion of
lead releases.
The deposited lead forms are largely insoluble. Lead accumulates in
the top few inches of leaf litter and soil. Runoff and erosion introduce
lead into surface waters as a suspended solid, which result in accumula-
tion of lead in the sediment.
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4-3.3.2 Pathway $2 — Solid Wastes, Tailings, and Municipal Landfill;
Solid Wastes,
Coal Piles and
Open Mines
\
«te.
Surface
Water j
Sediment
if
»
^ Ocean
/
Groundwater
Sources
In general, solid wastes containing lead are created by mineral ore
processing, iron and steel production, copper and zinc smelting, and the
production and"use of various lead-containing products. Pathway #2
describes the fate of lead in the environment as a result-of these sources,
The solid wastes result from the overburden of mining and low-grade
portions of mineral ore deposits. Tailings, which are highly concen-
trated in minerals, are produced as a final waste product of mineral
concentrating operations. Municipal waste landfills accumulate objects
containing lead, such as objects covered with lead-containing pigments,
or solder. Although lead batteries are the most obvious sources of lead
to municipal landfills, they are not a major contributor to lead concen-
trations in municipal dumps, because car batteries are generally recycled.
Mining of lead has been principally restricted to the state of
Missouri. The Old Lead Belt was found in the southeast portion of the
state and is currently inactive. The New Lead Belt (also referred to as
the Viburnum Trend), in the southwest portion of the state, has been first
in world lead production since 1970 (Wixson 1978). Since 1873, lead
mining has resulted in 1550 million metric tons of tailings, and 3875
million metric tons of combined tailings and waste (Martin and Mills
1976). Disposal of these wastes in the 19th and early 20th centuries
was without regard to environmental considerations, and thus erosion and
weathering contributed to adverse environmental impacts. Currently,
tailings are used to create dams for the establishment of tailing ponds.
The lead species in solid wastes and tailings depend on the nature of
the ore. Galena (PbS) is most commonly mined and is the most frequently
encountered form of lead in mine tailings. Other lead species include
PbO, PbC03 and PbS04 (Zimdahl and Hassett 1977, Jennett 1979).
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Acid Mine Drainage
Tailings and solid wastes from mineral mining aid in the formation
of mineralized acid drainage. The impact of acid mine drainage to local
surface waters largely depends on the alkalinity, or buffering capacity,
of the waters upstream or downstream of the point of discharge. The
streams channelling the Old and New Lead Belts are quite buffered and of
a neutral to slightly basic pH (Zimdahl and Hassett 1977, Wixson 1978).
Thus, rarely has lead in tailing etfluents been a problem in local screams
(Zimdahl and Hassett 1977). Most of the lead entering the streams is
associated with suspended solids in the form of PbS, PBC03, PbO and PbS04-
Fate Processes in Streams
Little evidence substantiates that surface mineralization in the
Lead Belts of Missouri has elevated levels of lead in the surface waters.
As stated earlier, most of the lead in the water column is in the
undissolved, particulate form. Lead in the Old Lead Belt enters the
streams principally via runoff and leaching through tailings (Wixson
1978). In the New Lead Belt region, the velocity of the streams is high
enough to prevent the suspended particulates from settling out.
Eventually, the streams discharge into Clearwater Lake, which is
about 30 miles from the last few mine discharges, and is dammed at one
end. The lead concentrations in Clearwater Lake sediments range from
<3 mg/kg at the point of stream entry to 60 mg/kg near the dam (Zimdahl
and Hassett 1977). Lakes with long narrow arms, such as Clearwater,
experience scour and washout during storms. The sediments are therefore
transported to the base of the dam. In this specific lake, the lake
sediments act as a temporary sink for heavy metals. Opening the dam
during periods of high in-flow, effectively removes the metals from the
lake sediments, thereby accounting for the low levels of lead found in
Clearwater Lake sediments (Wixson 1978, Zimdahl and Hassett 1977).
Coggins and co-workers (1979) investigated the drinking water
quality of the reservoir in the area engaged in lead and silver mining.
Lead concentrations were in the range 50-69 yg/1 in the water column.
Lead in the sediments averaged 150 mg/kg (ranging from 30-650 mg/kg),
which was principally adsorbed onto the clay fraction of the sediments.
Other metals were also associated with iron and manganese hydrous oxides,
or complexed with organic matter; for the most part, lead was not.
Groundwater Contamination from Tailings and Mining Activity
Mink (1972) investigated the groundwater of the Coeur d'Alene mining
area in Idaho. Evidence indicated that the effluent of a tailings pond
was not responsible for the high levels of lead found in the groundwater.
The aquifer pollution was a result of contact with tailings from old
abandoned mining operations. Solubilization of the heavy metals in the
tailings by the high water table resulted in concentrations of 6% lead
in the upper aquifer.
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Fly Ash Ponds
Disposal of fly ash generated from coal combustion has created
concerns about the leaching potential of metals associated with the fly
ash. Theis jȣ al. (1978) studied the extent of groundwater contaminations
from a fly ash pond. Analysis of the fly ash indicated that Pb was the
third most abundant heavy metal (after arsenic and zinc) in the flv ash
In the groundwater leachate, lead was generally found in the lowest
concentration of the metals tested, at about 40 ug/1, 100 feet from the
pond. Precipitation as the hydroxide and carbonate, rather than sorption
on the iron and manganese oxides controlled lead concentrations
(Theis _et al. 1978). The degree of precipitation is a function of pH.
Theis et al. (1978) show that abrupt precipitation of lead results at an
approximate pH of 6.5, thereby reducing the concentration of soluble Pb
from 10-^0 moles/1 at pH 6 to 10~6 moles/I at pH 7.
Municipal Landfills
Roulier (1975) conducted a study using soil from two sites to
examine municipal solid wastes disposal, and subsequent metal leaching.
At one site, conditions favored metal attenuation, and, at the other
landfill, a "worst case" scenario was simulated.
The first site collected leachate from 1.390 kilograms of municipal
refuse under anaerobic conditions in a soil column. The concentration
of lead was below the detection limit of 0.5 mg/1 and fell into the
category of "least generally mobile."
The second study used soil columns packed with quartz sand and
pure clay, and pure leachate was slowly passed from municipal landfills
through the columns. Under these conditions, 99.8% of the lead was atten-
uated by the soils, exceeding zinc, cadmium and mercury. The controlling
mechanism as in the fly ash study was precipitation at neutral to alka-
line pH ranges, and sorption to clays.
Data from other landfills show lead concentrations ranging from
0.1-2 mg/1, with less than 0.1 mg/1 as a typical value (U.S. EPA 1977b).
Another study of 12 landfills ranging in age from 0.25 to 16 years showed
a mean lead concentration in the leachate of 0.92 mg/1 (range 0.1-3.2 mg/1)
(Chian and DeWalle 1977); this is slightly under an order of magnitude
greater than the above study.
Lead in Soils from House Paint
Although lead from house paints contributes to localized high levels
of lead in the soils immediately surrounding a lead-painted house, on
the whole, this is not a significant source of lead to the land. Ranges
of 1000-2000 mg/kg in the soil have been reported (Bogden and Louria 1975)
Even though the concentration of lead in house paints is now controlled
older wooden houses may still be covered with leaded paint. Natural
weathering and sanding and scraping houses prior to repainting are ways
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in which lead is transferred to the soil. Bogden and Louria (1975)
analyzed the soil lead concentrations 15 and 30 meters away from a
repainted house, at the time of scraping the leaded paint, and one year
later. The lead concentration in the paint chips was 17%. The resul-
tant soil concentrations are shown below:
Lead Content at Various Distances from the House
Time Period
August 1973
August 1974
Control Soils
Concentration (mg/kg)
15 meters 30 meters
185
440
130-220
165
490
Summary
Thus far, the surface waters of the New Lead Belt do not show
elevated levels of lead. It is believed that the highly buffered,
neutral-to-basic nature of the streams channelling the New Lead belt
prevents the lead from solubilizing or settling out. Frequent
opening of the Clearwater Lake dam scours lead that settles onto the
lake sediments. Groundwater contamination from tailing ponds and fly
ash ponds does not appear to be a significant source of lead, although
it has occurred in some cases. Lead, in groundwater leachate is con-
trolled by precipitation as the hydroxide or carbonate, provided that
the pH is not acid. Municipal waste leachate studies categorize lead
in the least generally mobile metal group, where adsorption to clays and
precipitation control its movement.
4.3.3.3 Pathway #3 — Aqueous Industrial Discharge
Effluent
r
Aque.ous
Discharge
Treatment
Sludge
Hazardous Waste
Solid Waste Dump
Pathway
#4
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Sources
Sources of aqueous discharges of lead to the environment include
lead production, coal mining, and industries such as lead battery manu-
facture, paper and pulp and nonferrous metals production. Pathway #3
describes the fate of lead as a result of aqueous industrial discharge.
The lead battery industry is a major user of secondary lead and
recycles the wastewater to recover additional lead. Wastewater
treatment, as exercised by the lead battery industry, consists of a
settling tank, neutralization unit, in which lime, ammonia, or sodium
hydroxide is added to increase the pH; a scrubbing unit, which removes
dissolved carbon dioxide by aeration; and, finally, another settling
tank, to which coagulants are added to flocculate and precipitate the
suspended materials. Eventually, the sludge from both settling tanks
is collected, dewatered, and processed to recover the high lead content.
The effluent from the second settling tank is discharged to local surface
waters or POTWs (Chloride Overseas 1971). Fochtman and Mass (1972) found
that the lead content of several lead battery effluents ranged from
0.5 to 3.0 mg/1 dissolved lead, and from 5 to 35 mg/1 suspended lead.
The paper and pulp industry also discharges lead to water. This
discharge is principally a result of the lead-containing pigments on the
paper. Concentrations of lead in paper coating and glazing effluents
range from 0.05 to 1000 mg/1. After treatment and dilution, the average
lead concentration in the final effluent of 17 paper and pulp mills was
16 ug/1 (U.S. EPA 1979).
Distribution to Surface Waters
Mathis and Cummings (1973) and Mclntosh and Bishop (1976) have
studied the distribution of lead discharged into surface waters. The
Mathis and Cummings (1973) study used the Illinois River as its environ-
mental system. The river is known to receive both municipal and indus-
trial discharges. When compared with nonindustrial use (rural) rivers,
the average lead concentrations in the sediments of the Illinois River
(28 mg/kg) was 1.6 times that of the rural streams (17 mg/kg). The
water column contained an average of 0.002 mg/1 lead.
Mclntosh and Bishop (1976) researched the level of pollution in a
small eutrophic lake, which was the receptor of direct industrial
discharges primarily from metal plating and urban runoff. The metal
plating was discontinued in 1974; Mclntosh and Bishop (1976) examined
the changes in the lake in the tabulation of the data below. These
values represent averages, and thus the columns do not necessarily add:
Lead concentration (yg/1)
Water Column 1974 1975
Dissolved 24 9.4
Suspended 15.2 6.6
Total 28.6 14.4
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Of the ^4 water samples collected from Little Center Lake, dissolved
lead was detected (limit =2.0 ug/l) in only 50% of the samples and
suspended lead in only 18% of the samples. The lead, however, is quite
evident in the lake sediments. The top ten centimeters contained
between 450-500 mg/kg Pb dry weight. The highest concentration of lead
in the lake sediments was near the street sewer outfall, from which
suspended lead quickly settled out.
Sludge Disposal
The sludge generated by industrial effluent treatment is normally
disposed of in a solid or hazardous waste dump, or treated to recover
the lead, as in the battery industry. A properly designed landfill site
should prevent significant translocation of lead, which has a tendency
to precipitate in an insoluble state. Groundwater contamination is not
likely in a landfill or settling pond as the evidence in Pathway #2
suggests.
Ultimate Sinks
The sediments are the major sinks for lead discharged with indus-
trial effluent into surface waters. Treated industrial effluents
generate a waste sludge into which most of the lead partitions. Disposal
of the sludge at a hazardous or municipal landfill will generally prevent
further translocation of lead in the environment, with the exception of
runoff.
Summary
The manufacture of lead batteries could conceivably result in large
quantities of lead discharged into the environment. However, waste
effluent treatment practices, which have been effective since the early
1970s, have allowed little lead to be discharged via this route.
Studies of stream and lake systems receiving industrial discharge indi-
cate that the sediments concentrate most of the lead. Waste effluents
treated prior to discharge generate sludges that are disposed of in a
hazardous waste site. Mobilization is not generally expected to occur
from this site.
4-3.3.4 Pathway #4 — Publicly-owned Treatment Works
POTW Influent
— —
Primary
Treatment
\
-~
Biol.
Treatment
/
Sludge
-
Surface
Waters
—
Ocean
Incineration, Land
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Treatment Scheme
Pathway #4 describes the fate of lead in wastewaters that are
introduced into a publicly-owned treatment work (POTW). The inflow
to the POTW may be a combination of industrial and commercial effluents,
domestic wastes, and surface runoff. Consequently, the nature of the
influent is quite varied; however, typical influent lead concentrations
will be -0.1 mg/1 (Arthur D. Little, Inc. 1979).
The degree to which lead is removed from the raw wastewaters, and
thus the concentration of lead in the discharged x^astewaters, depends
on the type of treatment involved. The U.S. EPA (1977c) provides a
summary of data from 269 municipal treatment plants in the United States
that use various treatment methods. The data for lead are summarized in
Table 4-10.
Lead partitions into the sludge during treatment. Oliver and
Cosgrove (1974) found that lead immediately precipitates when introduced
to sewage. The metal exceeds others in this capacity.
Sludge Disposal
Sludge disposed onto land may go to a sanitary landfill, or be
spread for the purpose of amending the soil. The form of lead in sludge
is not exactly known. Sommers and co-workers (1976) found that lead
sulfides, phosphates, and hydroxides were not detected in sludges
containing relatively high concentrations of lead.
Sludge routed to municipal landfills was described in the section
on Pathway #2. Sludge that is incinerated will contribute to the con-
centrations of lead in the atmosphere. The fate processes will be
similar to those described in the discussion on Pathway //I.
Surface Water Discharge
The behavior of lead discharged with POTW effluents into local
surface waters will be similar to that already described for aqueous
pathways (Pathway #3). Morel and co-workers (1975) have provided a
detailed study of the fate of lead discharged by the Joint Water
Pollution Control Project (JWPCP) of the Los Angeles County Sanitation
District; these discharges may be generally representative of POTW
discharges to the ocean.1 Three equilibrium models were applied to
the sewage to determine the speciation of heavy metals present in the
sewage. Lead was present entirely as PbS in all models regardless of
the input of organic-complexing agents or adsorption surfaces.
Although lead was found in the fairly insoluble sulfide form in the
effluent (370 mgd effluent, discharged through submarine outfalls at a
-"-The wastes, containing both domestic and industrial wastes, contain
high levels of lead (250 mg/1) after primary treatment.
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TABLE 4-10. EFFLUENT DATA FROM U.S. MUNICIPAL TREATMENT
PLANTS USING VARIOUS TREATMENT METHODS
Type of Treatment
Primary
Biological (all types)
Activated sludge
Trickling filter
Biological with chemical addition
Tertiary
Effluent Data (Means)
% Removal
of Pb
24
38
39
37
39
44
Pb Concentration
(mg/1)
.136
.092
.067
.116
not available
not available
Source: U.S. EPA (1977c).
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depth of 60 meters), the studies indicated that the combined processes
of dilution and oxidation resulted in substantial solubilization of lead
(as well as other metals); this increases the residence time of lead in
the water and allows it to be transported greater distances.
Summary
The concentration of lead in POTW effluent, and the effectiveness
of its removal depends upon the initial influent concentration and type
of treatment enacted. Most of the lead partitions into the sludge
during treatment. Discharge to marine systems causes solubilization
of lead, which prohibits "hot-spots" because of dilution. In freshwaters,
lead is expected to largely partition into the sediments.
4.4 OVERVIEW
4.4.1 Atmospheric Levels and Pathways
The atmosphere receives the greatest portion (53%) of the total
environmental releases of lead; approximately 93% of these releases are
a result of automobile emissions. Transport of lead in the atmosphere
depends on particle size, chemical form, and the distribution and height
of the release. Particles larger than 20 ym are rapidly deposited.
Although automobile exhaust contains lead in extremely small aerosol
sizes, with a mass median diameter of 0.5 ym or less, large particles
may be released during cold start or acceleration. These larger par-
ticles are deposited onto the roadway, or within a few meters. Smaller
particles also are deposited, to some extent, near the roadway by
impaction; however, some fraction is carried a distance (<100 m)'from
heavily travelled roads and may be deposited by washout. Still, precipi-
tation may carry some of the particles a considerable distance; thus,
more remote areas may be contaminated.
Lead releases of smelter, fossil fuel combustion, and iron and
steel production are primarily from elevated point sources and are
generally less than 1 ym in size. Consequently, these particulates are
widely dispersed and are primarily deposited by precipitation. Smelter
emissions result in significant deposition of lead at distances up to
two miles from the smelter. Fugitive dusts account for higher deposition
near the source. Airborne releases from mining and milling operations
will largely be in the form of fugitive dusts, resulting in localized
deposition.
The deposited lead forms from all atmospheric sources are largely
insoluble. Lead accumulates in plants, leaf litter, and soil. Runoff
and erosion introduce lead into surface waters as a suspended solid,
which results in sediment concentration.
The monitoring data for lead generally reflect these fate pathways.
The range of lead levels in air for remote areas of the continental United
States is 0.0001-0.01 yg/m3. In contrast, urban areas show levels of
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0.5-10 yg/m3, which are considerably higher, primarily because of
automobile use. The monitoring data show rapid deposition; and it has
been estimated that lead levels in air generally decrease by about 50%
between 10 and 50 meters from the highway.
Elevated atmospheric lead levels are also found in the vicinity of
point sources, such as smelters, in the range of 0.4-4 yg/m3. Consi-
derably higher levels have been reported, however.
4.4.2 Aquatic Levels and Pathways
Direct sources of lead to water are largely unidentified; however,
they include such sources as iron and steel production, lead production,
and coal mining. Still, indirect sources, such as urban runoff and
atmospheric deposition, are significant sources to aquatic systems.
Lead reaching surface waters is likely to be strongly sorbed onto
suspended solids and sediments. Because lead in the sediment is strongly
sorbed, it is unlikely to be desorbed as a result of a physical distur-
bance. Changes in the water chemistry, for example, pH, could result
in an increased solubilization of lead. Lead found in the water columns
is expected to be strongly complexed by organic molecules. Lead can
bioconcentrate in aquatic organisms up to 2-4 orders of magnitude above
water concentrations. It appears to be fairly persistent in aquatic
biota, with a lifetime of at least several months. Little evidence
suggests biomagnification of lead in aquatic food chains.
Typical levels of lead in U.S. waters are less than 25 yg/1. Levels
of lead in seawater are considerably lower, on the order of 0.005 yg/1.
Lead concentrations in surface waters were higher in urban areas than in
rural areas.
Sediments contain considerably higher levels of lead than surface
waters. Coastal lead sediment contains approximately 100 mg/kg, while
the average lead in river sediments was estimated to be about 20 mg/kg.
Higher concentrations were found in STORET data, with mean concentrations
ranging from 27 to 267 mg/kg, during 1973-79.
4.4.3 Terrestrial Levels and Pathways
A large amount of lead (47%) enters the environment annually in the
form of solid waste, primarily from lead production and the disposal of
lead-containing products. In addition, a large amount of lead reaches
the soil as a result of atmospheric deposition.
Lead transported to soil is quite strongly sorbed, and, under most
conditions, is not subject to leaching. The movement of lead with the
erosion of soil particles is likely, however. Entrainment of soil
particles is also a possible route of lead transport. In addition,
uptake of lead into plants can occur, although only a small portion of
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the total lead in any soil is available for plant uptake. Bioconcen-
tration factors are generally less than 1, although they may be slightly
higher in the roots.
Because of the characteristics of the New Lead Belt, the production
of lead in that.area has apparently not resulted in elevated levels of
lead from tailings or solid wastes. The waters in the area are highly
buffered and neutral to basic. In addition, control of a dam in the
area prevents lead accumulation in the sediment of the immediate area
Groundwater contamination from tailing ponds and fly ash ponds does not
appear to be significant for lead, although it has occurred in some
cases.
Lead is common in municipal waste, because it is found in numerous
domestic and commercial products. However, its movement is controlled
by adsorption to clay and precipitation.
Monitoring data for lead in soils largely reflect airborne deposi-
tion patterns. An average concentration for lead in U.S. soils appears
to be about 20 mg/kg in uncontaminated soils. Elevated concentrations
are found in the vicinity of highways (up to 7600 mg/kg), and, in general,
in urban areas where a range of 100-800 mg/kg lead in soil is found.
Elevated concentrations are also found in the vicinity of smelters (up
to about 8000 mg/kg), in the vicinity of houses that at one time were
painted with lead-containing paints, and in old orchard soils. Urban
dust is also found to contain high levels of lead. Concentrations of
about 1000-1600 mg/kg are found in urban residential areas and 1400-
2400 mg/kg in commercial areas.
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REFERENCES
Adams, E.S. Effects of lead and hydrocarbons from snowmobile exhaust
on brook trout (Salvelinus fontinalis). Trans. Am. Fish. Soc. 104(2):
363-373; 1975.
Anderson, R.V. The effects of lead on oxygen uptake in the crayfish,
Oronectes virilis (HAGEN). Bull. Environ. Contain. Toxicol. 20:394-400;
1978.
Anderson, R.V.; Vinikour, W.S.; Brower, J.E. The distribution of Cd,
Cu, Pb and Zn in the biota of two freshwater sites with different trace
metal inputs. Holarctic Ecology 1:377-384; 1978.
Andren, A.W.; Lindberg, S.E.; Bate, L.C. Atmospheric input and geo-
chemical cycling of selected trace elements in Walker Branch Water Shed,
Oak Ridge, Tenn. Pub. No. 728. Oak Ridge, TN: Oak Ridge National
Laboratories; 1975. (As cited by U.S. EPA 1977a)
Armstrong, F.A.J.; Atkins, W.R.G. J. Mar. Biol. Assoc. UK 29:139-144;
1950. (As cited by Wong _et al. 1978)
Arthur D. Little Inc.; Sources of toxic pollutants in influents
to sewage treatment plants. IV. Integrated interpretation, part 1.
Washington, DC: U.S. Environmental Protection Agency; 1979.
Atkins, P.R.; Kruger, P. The natural removal of lead pollutants from a
suburban atmosphere. Technical Report No. 98. Standord, CA: Federal
Water Pollution Control Administration; 1968. (As cited by U.S. EPA
1977b)
Bagley, G.E.; Locke, L.N. The occurrence of lead in tissues of wild
birds. Bull. Environ. Contam. Toxicol. 2(5):297-305; 1967. (As cited
by U.S. EPA 1976)
Banus, M.; Valiela, I.; Teal, J.M. Export of lead from salt marshes.
Mar. Poll. Bull. 5(l):6-9; 1974. (As cited by U.S. EPA 1978)
Bell, M.A.; Ewing, R.A.; Lutz, G.A.; Holoman, V.L.; Paris, B.; Krause, H.H.
Reviews of the environmental effects of pollutants: VII. Lead. Cincinnati,
OH: U.S. Environmental Protection Agency; 1978.
Bertine, K.K.; Mendeck, M.P. Industrialization of New Haven, Connecticut,
as recorded in reservoir sediments. Environ. Sci. Technol. 12(2):201-207;
1978.
Bertinson, J.R.; Clark, C.S. Lead content of soils from urban housing.
Interface 6:1073-1076; 1973. (As cited by Nriagu 1978a)
Biggins, P.D.E.; Harrison, R.M. Chemical speciation of lead components
in streets dusts. Environ. Sci. Technol. 14(3):336-339; 1980.
Bogden, J.D.; Louria, D.B. Soil contamination from lead in paint chips.
Bull. Environ. Contam. Toxicol. 14(3):389-394; 1975. (As cited by
U.S. EPA 1978)
4-43
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I
I
I
I
I
I
I
I
I
I
I
I
I
I
Bolter, E.; Butz, T.; Arseneau, J.F. Geochemical effects of lead
smelters on the environment. Trace Substances in Environ. Health
9:107-112; 1975. (As cited by Nriagu 1978a)
Bowen, H.J. Trace elements in biochemistry. New York, NY: Academic
Press; 1966. 241 p. (As cited by Nriagu 1978a)
Bowen, V.T.; Sutton, D. J. Mar. Res. 10:153-167; 1951. (As cited bv
Wong et al 1978)
Bradford, G.R. Trace elements in the water resources of California.
Hilgardia 41:45-53; 1971. (As cited by Chow 1978a)
Bryan, E.H. Concentrations of lead in urban storm water. J. Water
Pollut. Control Fed. 46:2419-2431; 1974. (As cited by Chow 1978a)
Bryan, G.W.; Uysal, H. Heavy metals in the burrowing bivalve
Scrobicularia plana from the Tamar estuary in relation to environ-
mental levels. J. Mar. Biol. Assoc. 58:89; 1978. (As cited by Leland
.et al. 1979).
Chamberlain, A.C.; Clough, W.S.; Heard, M.J.; Newton, D.; Stott, A.N.B.;
Wells, A.C. Uptake of inhaled lead from motor exhaust. Postgrad. Med.
J. 51:790-794; 1975. (As cited by U.S. EPA 1977a)
Chau, Y.K.; Wong, P.T.S.; Bengert, G.A.; Kramar, 0. Determination of
tetraalkyllead compounds in water, sediment, and fish samples. Analvt
Chem. 51(2):186-188; 1979.
Chian, E.S.K.; DeWalle, F.B. Evaluation of leachate treatment. Vol. 1.
Characterization of leachate. Report No. EPA-6001-2-77-186a. Washington,
DC: U.S. Environmental Protection Agency; 1977.
Chisolm, D.; Bishop, R.E. Phytoprotection 48:78-81; 1967. (As cited by
Nriagu 1978a)
Chloride Overseas, Ltd. Effluent treatment at battery factories. The
Battery Man 8; 1971.
Cholak, J.; Schafer, L.J.; Sterling, T.D. Atmospheric concentrations of
lead. J. Air Pollut. Contr. Assoc. 11:281-288; 1961. (As cited by
Nriagu 1978a)
Chow, T.J. Isotope analysis of seawater by mass spectrometry. J. Water
Poll. Contr. Fed. 40(3,Pt.l):399-411; 1973.
Chow, T.J. Lead in the hydrosphere. Pure & Appl. Chem. 50:395:405; 1978.
Chow, T.J. Lead in natural waters. Nriagu, J.O. ed. The biogeochemistry
of lead in the environment. New York, NY: Elsevier/North Holland Bio-
medical Press; 1978a.
4-49
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Chow, T.J.; Earl, J.L. Lead and uranium in Pennsylvania anthracite.
Science 169:577-580; 1970. (As cited by Nriagu 1978 a)
Chow, T.J.; Earl, J.L.; Snyder, C.B. Lead aerosol baseline: concentra-
txon at White Mountain and Laguna Mountain, California. Science 178
(4059):401-402; 1972.
Chow, T.J.; Bruland, K.W.; Bertine, K.; Soutar, A.; Koide, M. ;
Goldberg, E.D. Lead pollution. Records in Southern California
sediments. Science 181:551-552; 1973. (As cited in Nriagu 1978a)
Chow, T.J.; Snyder, C.B.; Earl, J.L. In: Isotope ratios as pollutant
source and behavior indicators. Vienna: IAEA; 1975. 95-108. (As
cited by Nriagu 1978a)
Clark, D.R. Lead concentrations: bats vs. terrestrial small mammals
collected near a major highway. Env. Sci. Technol. 13(3):338-341; 1979.
Coggins, A.J.; Tuckwell, K.D.; Byrne, R.E. An investigation of the
heavy metal content of the water and sediments in a reservoir supplv
drinking water to a major mining center. Environ. Sci. Technol. 13(10)-
1281-1285; 1979.
Colucci, J.M.; Begeman, C.R.; Kumler, K. Lead concentrations in Detroit,
New York, and Los Angeles air. J. Air Pollut. Contr. Assoc. 19:255-260;
1969. (As cited by Nriagu 1978b)
Connor, J.J.; Shacklette, H.T. Background geochemistry of some rocks,
soils, plants, and vegetables in the conterminous United States.
Washington, DC: U.S. Geological Survey Professional Paper 574-F; 1975.
(As cited by U.S. EPA 1978)
Corrin, N.L.; Natusch, D.F.S. Physical and chemical characteristics of
environmental lead. In: Lead in the environment. Washington, DC:
National Science Foundation; 1977:7-31.
DeTreville, R.T.P. Natural occurrence of lead. Arch. Environ. Health
8:212; 1964. (As cited by Zimdahl and Hassett 1977)
Drifmeyer, J.E.; Odum, W.E. Lead, zinc, and manganese, in dredge-spoil
pond ecosystems. Environ. Conserv. 2(l):39-45; 1975.
Durum, W.H.; Hem, J.D.; Heidel, S.G. Reconnaissance of selected minor
elements in surface waters of the United States. U.S. Geol. Survey
Circular 643; 1971. 49 p. (As cited by Chow 1978a)
4-50
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Edgington, D.N.; Robbins, J.A. Records of lead deposition in Lake
Michigan sediments since 1800. Environ. Sci. Technol. 10:266-274- 1976
(As cited by Chow 1978)
Elfving, D.C.; Haschek, W.M.; Stehn, R.A.; Bache, C.A.; Lisk, D.J.
Heavy metal residues in plants cultivated on and in small mammals
indigenous to old orchard soils. Arch. Environ. Health, pp. 75-99-
March/April 1978.
Elfving, D.C.; Bache, C.A.; Lisk, D.J. Lead content of vegetables,
millet, and apple trees grown on soils amended with colored newsprint.
J. Agric. Food Chem. 27(1):138-140; 1979.
Elias, R.W.; Hinkley, T.; Hirao, Y.; Patterson, C. Geochim. Cosmochim.
Acta 40:583; 1976. (As cited by Settle and Patterson 1980)
Fitchko, J.; Hutchinson, T.C. A comparative study of heavy metal con-
centrations in river mouth sediments around the Great Lakes. J. Great
Lakes Res. 1:46-78; 1975. (As cited by Rickard and Nriagu 1978)
Fleischer, M. In: Cycling and control of metals. Curry, M.G.;
Gigliotti, G.M. eds. Proc. Environ. Resource Conf., Cincinnati, OH:
National Environ. Res. Center; 1973. 3-10. (As cited by Chow 1978)
Fochtman, E.G.; Haas, W.R. Evaluation of lead plant x^astewater treat-
ment methods. Denver, CO: Battery Council International Convention;
1972.
Gale, N.L.; Wixson, B.C. Cadmium in forest ecosystems around lead
smelters in Missouri. Env. Health Persp. 28:23-37; 1979.
Gale, N.L.; Wixson, G.G.; Hardie, M.G.; Jennett, J.C. Aquatic organisms
and heavy metals in Missouri's Jew Lead Belt. Water Resources Bull
9:673-688; 1973.
Giles, F.E.; Middleton, S.G.; Grau, J.G. Evidence for the accumulation
of atmospheric lead by insects in areas of high traffic density. Environ.
Entomol. 2(2):299-300; 1973. (As cited by U.S. EPA 1978)
Gire, M.P., Narbonne, J.F.; Serfaty, A. J. Europ. Toxicol. 7-98-103-
1974. (As cited by Wong jet_ al. 1978)
Gish, C.D., Christensen, R.E. Cadmium, nickel, lead, and zinc in earth-
worms from roadside soil. Environ. Sci. Technol. 7(11):1060-1062- 1973
(As cited by U.S. EPA 1978)
Graham, D.L. Trace metal levels in intertidal mollusks of California.
Veliger 14(4):365-372; 1972. (As cited by U.S. EPA 1978)
4-51
-------
Gullvag, B.M. Subcellular localization of polluting metals in roadside
earthworms exposed to traffic exhaust gases. Cytobios 22:141-153; 1978.
Habibi, K. Characterization of particulate matter in vehicle exhaust.
Environ. Sci. Technol. 7(3):223-234; 1973.
Hardisty, M.W. ; Kortar, S. ; Sainsbury, M. Man. Pollut. Bull. 5:61-63;
1974. (As cited by Wong et al. 1978)
Harrison, G.F. The caviat incident. In: Proceedings of the inter-
national experts discussion on lead — occurrence, fate and pollution
in the marine environment. Rovini, Yugoslavia; 1977.
Harrison, R.M.; Laxen, D.P.H. Sink processes for tetraalkyllead com-
pounds in the atmosphere. Environ. Sci. Technol. 12(13):1384-1392;
1978.
Harrison, R.M.; Perry, R. The analysis of tetraalkyllead compounds and
their significance as urban air pollutants. Environ. Sci.'Technol.
ll(9):847-852; 1977.
Haschek, W.M.; Lisk, D.J.; Stehn, R.A. Accumulation of lead in rodents
from two old orchard sites in New York. Washington, DC: National
Academy of Sciences; 1979:192-199..
Hemphill, D.D.; Marienfeld, C.J.; Reddy, R.S.; Heidlage, W.D.; Pierce, J.O.
Toxic heavy metals in vegetables and forage grasses in Missouri's lead
belt. J. AOAC 56(4):974-988; 1971.
Hirao, Y.; Patterson, C.C. Lead aerosol pollution in the High Sierras
overrides natural mechanisms which exclude lead from a food chain.
Science 184:989-992; 1974.
Holcombe, G.W.; Benoit, D.A.; Leonard, E.N.; McKim, J.M. Long-term
effects of lead exposure on three generations of brook trout (Salvelinus
fontinalis). J. Fish. Res. Board Can. 33(8):1731-1741; 1976.
Huang, C.P.; Elliott, H.A.; Ashmead, R.M.; Interfacial reactions and the
fate of heavy metals in soil-water systems. J. Water Poll. Contr. Fed.
49(5):745-756; 1977.
Hutchinson, .T.C. Lead pollution, the automobile and health. Publ. No.
EF-5. Toronto: University of Toronto, The Institute of Environmental
Sciences and Engineering; 1973:1-10.
Iskander, I.K.; Keeney, D.R. Environ. Sci. Technol. 8:165-170; 1974.
(As cited by Nriagu 1978a)
4-52
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Jackson, D.R.; Watson, A.P. Disruption of nutrient pools and transport
of heavy metals in a forested watershed near a lead smelter. J. Environ.
Qual. 6(4):331-338: 1977.
Jennett, J.C.; Foil, J.L. Trace metal transport from mining, milling
and smelting watersheds. JWPCF 51(2):378-404; 1979.
Jennett, J.D.; Linnemann, S.M. Disposal of lead and zinc containing
wastes on soils. J. Water Poll. Contr. Fed. 49(8):1842-1856; 1977.
Jennett, J.C.; Wixson, B.C.; Lowsley, I.H.; Purushothaman, K.; Bolter, E. ;
Hemphill, D.D.; Gale, N.L.; Tranter, W.H. Transport and distribution from
mining, milling and smelting operations in a forest ecosystem. In: Lead
in the environment. Washington, DC: National Science Foundation; 1977:
135-178.
Kahn, M.A.Q.; Coello, W.F.; Saleem, Z.A. Lead content of soils along
Chicago's Eisenhower and Loop-Terminal expressways. Arch. Environ.
Contain. Toxicol. 1 (,3): 209-223; 1973. (As cited by U.S. EPA 1978)
Kauranen, P.; Jarvenpaa, T. Biological half-times of 210po and 210PB
in some marine organisms. Annual Report. Helsinki: University of
Helsinki, Department of Radiochemistry; 1972. (As cited by Wong et al.
1978)
Kemp, A.L.W.; Dell, C.I. A preliminary comparison of the composition of
bluffs and sediments from Lake Ontario, Erie, and Huron. Can. J. Earth
Sci. 13:1070-1081; 1976. (As cited by Nriagu 1978a)
Kleinsman, M.T.; Kneips, T.J.; Berstein, D.M.; Eisenbud, M. Fallout of
toxic trace metals in New York City. Drucker, H.; Wildung, R.E. eds.
Biological implications as metals in the environment. Proceedings of
the fifteenth annual Hanford life science symposium; at Richland WA
September 26, 1977.
Koeppe, D.E. The uptake, distribution and effect of cadmium and lead
in plants. The Sci. Total Environ. 7(3):197-206; 1977.
Koirtyohann, S.R.; Wixson, B.C.; Edwards, H.W. Krenkel, P.A. ed. Heavy
metals in the aquatic environment. New York, NY: Pergamon Press; 1975:
243-246.
Kopfler, F.C.; Mayer, J. Concentrations of five trace metals in the
waters and oysters of Mobile Bay, Alabama. Proc. Natl. Shellfish Assoc.
63:27-34; 1973. (As cited by U.S. EPA 1978)
Kopp, J.F. Hemphill, D.C. ed. Trace substances in environmental health.
Columbia, MO: University of Missouri; 1969: 111:59.
Kopp, J.F.; Kroner, R.C. Trace metals in waters of the United States.
Cincinnati, OH: Federal Water Pollution Control Administration; 1967.
4-53
-------
Korninga, P. Quart. Rev. Biol. 27: 266-308; 1952 (As cited by Wong et al
1978).
Lagerwerff, J.V. In: Agriculture and the quality of our environment.
Publ. No. 85. Washington, DC: American Association for the Advancement
of Science; 1967. (As cited in Zimdahl and Hassett 1977)
Laveskog (1971), A method for determining tetrancthyl lead (T1IL) and
tetraethyl lead (TEL) in air. Proceedings of the Second International
Union of Air Pollution Prevention Associations, Washington, DC. Paper
No-CP-371). New York, New York: Academic Press; 1971: 549-557 (As cited
by USEPA 1977a).
Lazrus, A.L.; Lorange, E.; Lodge, J.P. Jr. Lead and other metal ions in
United States precipitation. Environ. Sci. Technol. 4:55-58; 1970.
(As cited in Chow 1978a)
Lehninger, A.L. Biochemistry. New York, NY: Worth Publishers, Inc.;
1970. 833 p.
Leland, H.V.; McNurney, J.M. Lead transport in a river ecosystem.
Preprint of paper presented at the international conference on transport
of persistent chemicals in aquatic ecosystems. National Research Council
of Canada; 1974.
Leland, H.V. est _al. Bioaccumulation and toxicity of heavy metals and
related trace elements. J. Water Poll. Contr. Fed. 51(6):1592-1616-
1979.
Little, P.; Martin, M.H. A survey of zinc, lead and cadmium in soil
and natural vegetation around a smelting complex. Environ. Pollut.
3:241-254; 1972. (As cited by U.S. EPA 1977a)
Livingstone, D.A. Fleischer, M. ed. Data of geochemistry. 6th ed.
U.S. Geol. Survey Prof. Paper No. 440-G; 1964. 64 p. (As cited by
Chow 1978)
Mancy, K.H. ed. Instrumental analysis for water pollution control.
Ann Arbor, MI: Ann Arbor Science; 1971. 343 p. (As cited by
Chow 1978)
Marietta, G.P.; Gabrielli, L.F.; Favretto, L. Pollution of mussels by
particulate lead from sea water. Z. Lebensm. Unters. Forsch 168:181-184;
Martin, H.W.; Mills, W.R. Water pollution caused by inactive ore and
mineral mines ~ a national assessment. Cincinnati, OH: U. S.
Environmental Protection Agency; 1976. Available from NTIS, Springfield,
VA; So 264 956.
4-54
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Martin, W.E. Mercury and lead residues in starlings — 1970. Pest
Monit. J. 6(l):27-32; 1972. (As cited by U.S. EPA 1978)
Mathis, B.J.; Cummings, T.F. Distribution of selected metals in bottom
sediments. J. Water Pollut. Contr. Fed. 45(7):1573-1583; 1973 (As •
cited by Chow 1978)"
Mclntosh, A.; Bishop, W. Distribution and effects of heavy metals —
a contaminated lake. Publ. No. 85. Lafayette, IN: Purdue University,
Water Resources Research Center; 1976.
McMullen, T.P.; Faoro, R.B.; Morgan, G.B. Profile of pollutant faction
in nonurban suspended particulate matters. J. Air Pollut. Contr. Assoc
20:369-372; 1970. (As cited by U.S. EPA 1978c)
Mink, L.L.; Williams, R.E.; Wallace, A.T. Effect of early day mining
operations on present day water quality. Groundwater 10(l):17-26; 1972.
Mor, E.D.; Beccaria, A.M. A dehydration method to avoid loss of trace
elements in biological samples. In: Proceedings of international
experts discussion on lead — occurrence, fate and pollution in the
marine environment. Rovini, Yugoslavia; 1977.
Morel, F.M.M.; Westall, J.C.; O'Melia, C.R.; Morgan, J.J. Fate of trace
metals in Los Angeles County Wastewater Discharge. Environ Sci
Technol. 9(8):756-761; 1975.
Motto, H.L.; Daines, R.H.; Chilko, D.M.; Motto, C.K. Lead in soils and
plants: its relation to traffic volume and proximity to highways
Environ. Sci. Technol. 4:231-237; 1970. (As cited by Nriagu 1978a)
Namminga, H.E.; Scott, J.E.; Burks, S.L. Proc. Okla. Acad. Sci. 54:62-
64; 1974. (As cited by Wong et al. 1978)
National Academy of Sciences (NAS). Airborne lead in perspective.
Washington, DC: National Academy of Sciences; 1972. 29 p. (As cited
Dy U • o • EjrA 1978)
Newton, C.D.; Shepard, W.W.; Coleman, M.S. J. Water Pollut. Contr Fed
46:999-1000; 1974. (As cited by Chow 1978a)
• Nriagu, J.O. Lead in soils, sediments and major rock types NriAo,, T n
• ed The biogeochemistry of lead in the environmentParTI.' EcoScai
cycles. New York, NY: Elsevier/North-Holland Biomedical Press; 1978^
I
I
I
4-55
-------
Nriagu, J.O. Lead in the atmosphere. Nriagu, J.O. ed. The biogeochem-
istry of lead in the environment. Part A. Ecological cycles. New York,
NY. Elsevier/North-Holland Biomedical Press; 1978b: 137-184.
O'Brien, J.; Barry, E.F.; Rei, M.T.; Reynolds, H.H. Atmospheric lead
content of eastern Massachusetts. Environ. Lett. 8:297-302; 1975.
(As cited by Nriagu 1978b)
Oliver, B.C.; Cosgrove, E.G. The efficiency of heavy metal removal by
a conventional activated sludge treatment plant. Water Res. 8(11)-
869-874; 1974.
Olson, K.W.; Skogerboe, R.K. Identification of soil lead compounds from
automotive sources. Environ. Sci. Technol. 9(3):227-230; 1975. (As
cited by U.S. EPA 1977a)
Page, A.L.; Ganje, T.J. Accumulations of lead in soils for regions of
high and low motor vehicle traffic density. Environ. Sci. Technol.
4:140-142; 1970. (As cited by Nriagu 1978a)
Pagenkopf, G.K.; Neuman, D.R. Lead concentrations in native trout.
Bull. Environ. Contain. Toxicol. 12(l):70-75; 1974.
Pakkala, I.S.; White, M.N.; Burdick, G.E.; Harris, E.G.; Lisk, D.J.
A survey of the lead content of fish from 49 New York State waters.
Pestic. Monit. J. 5:348.355; 1972. (As cited by Bell et al 1979).
Patterson, C.C. Lead. Arch. Environ. Health 11:344-360; 1965. (As
cited by Nriagu 1978b)
Patterson, C.C. Mar. Chem. 2:69:84; 1974. (As cited by Chow 1978a)
Patterson, C.C.; Settle, D.; Glover, B. Analysis of lead in polluted
coastal seawater. Mar. Chem. 4:305-319; 1976. (As cited by Chow 1978)
Perhac, R.M. Water transport of heavy metals in solution and by differ-
ent sizes of particulate solids. Research Report No. 32. Knoxville,
TN: Tennessee University, Water Resources Research Center; 1974.
Available from: NTIS, Springfield, VA; PB 232 427.
Peterson, J.O. A study of lead in lake sediments. Thesis, Univ. of
Wisconsin, Madison, 1973. (As cited by Nriagu 1978a)
Peterson, P.J. Lead and vegetation. Nriagu, J.O. ed. The biogeochemi-
stry of lead in the environment. Part A. Ecological cycles. New York,
NY: Elsevier/North-Holland Biomedical Press; 1978.
4-56
-------
I
I
•Phillips, G.R.; Russo, R.C. Metal bioaccumulation in fishes and aquatic
invertebrates: a literature review. Report No. EPA-600/3-78-103.
Washington, DC: U.S. Environmental Protection Agency 1978
I
I
I
I
I
I
I
I
I
I
I
I
|
T^°1^e: ^•^1; Haney' A> Institute of Environmental Studies Report No
UILU-IES-75-0001. Urfaana, IL: University of Illinois; 1975. 133 n
• (As cited by Nriagu 1978a) P<
I
I
Price, R.E.; Knight, L.A. Mercury, cadmium, lead, and arsenic in sedi-
ments, plankton, and clams from Lake Washington and Sardis Reservoir
Mississippi. Pest. Monit. J. 11(4):182-189; 1978.
Price, P.W.; Rathcke, B.J.; Gentry, D.A. Lead in terrestrial anthropoH-
evidence for biological concentration. Environ, Entomol. (3)- 370-372-
1974. (As cited in U.S. EPA 1978)
Pringle, B.H.; Hissong, D.E.; Katz, E.L.; Mulawka, S.T. Trace metal
accumulation by estuarine mollusks. J. Sanit. Eng. Div. Am. Soc. Civ.
Eng. 94:455-475; 1968. (As cited by Wong e£ al. 1978)
Proctor, P.O.; Kisvarsanyi, G.; Garrison, E.; Williams, A. Hemphill, D.D.
ed. Trace substances in environmental health. VII. Columbia, MO: Univer-
sity of Missouri; 1974: 57-61.
Ragaini, R.C.; Ralston, H.R.; Roberts, N. Environmental trace metal
contamination in Kellogg, Idaho, near a lead smelting complex. Environ.
Sci. Technol. 11(8):773-781; 1977.
Rameau. J. Th. L.B. In: Environmental health aspects of lead.
Luxembourg: Commission of European Communities; 1973: 189-197.
(As cited by Nriagu 1978a)
Ray, S. Bioaccumulation of lead in Atlantic salmon (Salmo salar).
Bull. Environ. Contam. Toxicol. 19:631-636; 1978.
Reichert, W.L.; Federighi, D.A.; Malins, D.C. Uptake and metabolism of
lead and cadmium in coho salmon (Qncorhynchus kisutch). Comp. Biochem.
Physiol. 63C:229-234; 1979.
Rickard, D.T.; Nriagu, J.O. Aqueous environmental chemistry of lead.
Nriagu, J.O. ed. The biogeochemistry of lead in the environment. Part A.
Ecological cycles. New York, NY: Elsevier/North Holland Biomedical
Press; 1978: 219-283.
, R.D.; Johnson, M.S.; Hotton, M. Environ. Pollut. 15-61-69-
(As cited by Clark 1979) 9'
4-57
-------
Roulier, M.H. Research on containment movement in soils. Cincinnati,
OH: U.S. Environmental Protection Agency; 1975.
Sartor, J.D.; Boyd, G.B. Water pollution aspects of street surface
contaminants. Report No. EPA-R2-72-081. Washington, DC: U.S. Environ-
mental Protection Agency; 1972.
Scanlon, P.F. Lead contamination of mammals and invertebrates near
highways with different traffic volumes. Washington, DC: National
Academy of Sciences; 1978.
Scanlon, P.F.; O'Brien, T.G.; Schauer, N.L.; Coggin, J.L.; Steffen, D.E.
Bull. Environ. Contain. Toxicol. ; 1978. (As cited by Scanlon et al.
1979)
Scanlon, P.F.; O'Brien, T.G.; Schauer, N.L.; Oderwald, R.G. Lead
levels in primary feathers of American woodcocks harvested by hunters
throughout the United States range. Bull. Environ. Contain. Toxicol.
21:683-688; 1979.
Schell, W.R.; Barnes, R.S. Rubin, A.J. ed. Aqueous environmental
chemistry of metals. Ann Arbor, MI: Ann Arbor Science Publishers;
1974: 129-169. (As cited by Wong et al. 1978)
Schlesinger, W.H.; Reiners, W.A.; Knopman, D.S. Heavy metal concentra-
tions and deposition in bulk precipitation in montane ecosystems of New
Hampshire, USA. Environ. Pollut. 6:39-47; 1974. (As cited by Chow
1978)
Schroeder, H.A. The poisons around us. Bloomington, IN: Indiana Uni-
versity Press; 1974. (As cited by Nriagu 1978a)
Schubert, J. Chemical specificity in biological interactions. Gurd, R.N.
ed. New York, NY: Academic Press; 1954: 114-163.
Schuck, E.A.; Locke, J.K. Relationship of automotive lead particulates
to certain consumer crops. Environ. Sci. Technol. 4(4):324-330; 1970.
Schulz-Baldes, M. Mar. Biol. 25:177-193; 1974. (As cited by Wong et al.
1978)
Schwimer, S.R. Trace metal levels in three subtidal invertebrates.
Veliger 16(1):95-102; 1973. (As cited by U.S. EPA 1978)
Sehmel, G.A.; Hodgson, W.H. Predicted dry deposition velocities.
Proceedings of the synposium on atmosphere — surface exchange of
particulate and gaseous pollutants. ERDA Symposium Series 38. Richland,
WA; 1976: 399-422. (As cited by U.S. EPA 1978).
Serne, R.J. Geochemical distribution of selected trace metals in San
Francisco Bay sediments. Drucker, H.; Wildung, R.E. eds. Biological
implications of metals in the environment; 1977.
4-58
-------
I
I
I
I
I
I
I
I
Settle, D.M. ; Patterson, C.C. Lead in albacore: guide to lead pollution
in Americans. Science 207:1167-1176; 1980.
Siccania, T.G. ; Smith, W.H. ; Mader, D.L. Changes in lead, copper, dry
and weight and organic matter content of the forest floor of white pine
stands in central Massachusetts over 16 years. Environ. Sci. Technol
14(l):54-56; 1980.
Smith, W.H. Metal contamination of urban woody plants. Environ. Sci.
Technol. 7:631; 1973. (As cited by Smith 1976)
Smith, W.H. Lead contamination of the roadside ecosystem. J. Air
Pollut. Contr. Assoc. 26(8) : 753-766; 1976.
Sommers, L.E.; Nelson, D.W. ; Terry, R.E.; Silviera, D.J. Nitrogen and
metal contamination of natural waters from sewage sludge disposal on
land. Lafayette, IN: Purdue University, Resources Research Center; 1976.
Spehar,_R.L.; Anderson, R.L.; Fiandt, J.T. Toxicity and bioaccumulation
ot cadmium and lead in aquatic invertebrates. Environ. Pollut. 15:195-
ZUo ; 1978.
Stenner, R.D.; Nickless, G. Mar. Pollut. Bull. 6-89-92- 197S a • ,
by Wong et. _al. 1978) »"•>-•>.• o.oy yz, iy/5. (As cited
_
•
•
•
•
I
I
I
I
Stevenson F.J.; Welch, L.F. Migration of applied lead in field soil.
Environ. Sci. Technol. 13(10) .-1255-1259; 1979.
Struempler, A.W. Trace element composition in atmospheric particulates
?0-3l837 1Q7*d th(l SUmme; f 19?4 at Chadr°n' Neb"*ka. Atmos. Environ.
10.33-37; 1976. (As cited by Nriagu 1978b)
Summers, A.O ; Silver, S. Microbial transformations of metals. Ann.
Rev. Microbiol. Annual Reviews, Inc; 1978.
.' L'S' A SUrVey °f air and Population lead levels in
selected American communities. Final Report. Cincinnati, OH: U.S.
environmental Protection Agency; 1972: 1-73.
of ™~*°™ *~* P«tlcl«.
: ""' J'N': Brandt> "• Compositio,, size and
. Contr. Assoo.
4-59
-------
Ter Haar, G. ; Aronow, R. New information on lead in dirt and dust as
related to the childhood lead problem. Environ. Health Persp. 7:83-89;
J* j I Q •
Theis, T.L.; Richter, R.O. Chemical speciation of heavy metals in power
plants ash pond leachate. Environ. Sci. Technol. 13(2)':219-228; 1972.
Theis, T.L. ; Westrick, J.D.; Hsu, C.L.; Marley, J.J. Field investigation
of trace metals in groundwater from fly ash disposal. J. Water Pollut
Contr. Fed. 50(11) : 2457-2469; 1978.
Thomas, Personal communication; 1976. (As cited by Nriagu 1978a)
Tolonen K ^*** °f heavy metals on two roadside bogs in Finland.
Suo 25:77-84; 1974. (As cited by Nriagu 1978a)
long S.C.; Young, W.D.; Gutermann, Witt,; Lisk, D.C. Trace Metals in
Lake Cayuga lake trout (Salvelinus namaycush) in relation to a*e
J. Fish Res. Bd. Can. 31:238-239; 1974 (As cited by Bell et al°1979).
-*.S. Department of the Interior (U.S. DI) . Nontoxic shot regulations
for hunting water foul, 1980-1981. Washington D.C. : Fish and Wildlife
Service, U.S. Department of the Interior, 1979.
U.S. Environmental Protection Agency (U.S. EPA) Helena Valley Montana,
area environmental pollutant study. Publication No. AP-91. Research
Triangle Park, NC: Office of Air Programs, U.S. Environmental Protection
Agency; 1972 (As cited in U.S. EPA 1978).
U.S. Environmental Protection Agency (U.S. EPA). Air quality criteria
for lead. Report No. EPA 600/8-77-017. Washington, DC: U.S. Environ-
mental Protection Agency; 1977a.
U.S. Environmental Protection Agency- (U.S. EPA). The prevalence of sub-
surface migrations of hazardous chemical substances at selected indus-
trial waste disposal sites. Washington, DC: U.S. Environmental Protec-
tion Agency; 1977b.
U.S. Environmental Protection Agency (U.S. EPA). Information for proposed
general pretreatment regulations. EPA Report No. 40 CFR 403. Washington,
DC: U.S. Environmental Protection Agency; 1977c.
U.S. Environmental Protection Agency (U.S. EPA). Reviews of the environ-
mental effects of pollutants: VII. Lead. Washington, DC: Office of
Research and Development, U.S. Environmental Protection Agency; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Development document
for effluent limitations guidelines and standards for the pulp and paper
industry. Washington, D.C.: Effluent Guidelines Division, U.S.
Environmental Protection Agency; 1979.
4-60
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
U.S. Environmental Protection Agency (U.S. EPA). STORET. Washington,
DC: Monitoring and Data Support Division, U.S. Environmental Protection
Agency; 1980.
Varanasi, U.; Gmur, D.J. Influence of water-borne and dietary calcium
on uptake and retention of lead by coho salmon (Oncorhynchus kisutch).
Toxicol. Appl. Pharm. 46:65-75; 1978.
Versar, Inc. Statement of probable fate of lead. McLean, VA: Versar,
Inc. 1979.
Vuceta, J.; Morgan, J.J. Chemical modeling of trace metals in fresh-
waters: role of complexation and adsorption. Environ. Sci. Technol.
12(12):1302-1308; 1978.
Ward, N.I.; Reeves, R.D.; Brooks, R.R. Effect of lead from motor vehicle
exhausts on trees along a major thoroughfare in Palmerston North, New
Zealand. N.Z. J. Sci. 18:261-267; 1975.
Warren, H.V. Biogeochemical prospecting for lead. Nriagu, J.O. ed.
The biogeochemistry of lead in the environment. Part A. Ecological
cycles. New York, NY: Elsevier/North Holland Biomedical Press; 1978.
Warren, H.V.; Delavault, R.E.; Fletcher, K.W. Copper, zinc, and lead
content of trout livers as an aid in the search for favorable areas to
prospect. Can. Mining Metall. Bull. 64:34-45; 1971. (As cited by
Nriagu 1978a)
Williams, R.J.P. Biol. Rev. 28:381-415; 1953. (As cited by Wong et al.
1978)
Wixson, B.C. Biogeochemical cycling of lead in the new lead belt of
Missouri. Nriagu, J.O. ed. The biogeochemistry of lead in the environ-
ment. Part B. Biological effects. New York, NY: Elsevier/North
Holland Biomedical Press; 1978:119-136.
Wong, P.T.S.; Silverberg, B.A.; Chau, Y.K.; Hodson, P.Y. Lead and the
aquatic biota. Nriagu, J.O. ed. The biogeochemistry of lead in the
environment. Part A. Ecological cycles. New York, NY: Elsevier/i
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Zimdahl, R.L.; Koeppe, D.E. Uptake by plants. Boggess, W.R.; Wixson,
B.C. eds. Lead in the environment. Washington, DC: The National
Science Foundation; 1977: 99-104.
Zimdahl, R.L.; Hassett, J.J. Lead in soil. Boggess, W.R.; Wixson, B.C.
eds. Lead in the environment. Washington, DC: The National Scienc*
Foundation; 1977: 93-98.
Zimdahl, R.L.; McCreary, D.T.; Gwynn, S.M. Lead uptake by plants -
the influence of lead source. Bull. Environ. Contain. Toxicol. 431-435-
-Ly / o •
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5.0 HUMAN EFFECTS AND EXPOSTTRE
5.1 HUMAN TOXICITY
5.1.1 Introduction
_ The human health effects of lead have been extensively and inten-
8^^"V!!Sf"fd; *^:Jeveral ""P-hensive reviews of lead toxi-
S«trr/ae i977' U'S' EPA 19?7' Nria§U 1978>" ^ne of the
literature, however, has demonstrated any natural function of lead in the
body nor any beneficial effects. However, its pervasive nature in the
environment makes some degree of exposure inevitable. This chapter is
focused primarily on toxicity data that are most useful in the assessment
of human exposure to lead and the consequences of such exposure.
The heme-hematopoietic system, the kidney, and the nervous system
Rare the three organ systems that are major targets of lead toxicosis.
Subtle neuro-behavioral impairments, such as difficulty in task perfor-
mance, have also recently been reported at blood lead levels at which no
other symptoms of lead toxicity are seen. These findings have resulted
| in some uncertainty in the established maximal permissible daily intake
• level for lead. In 1972, a joint FAO/WHO committee established' a provi-
sional tolerable weekly intake of 3 milligrams for adults (Mahaffey
1Ue °f,?'? milliSrams lead is currently considered the maximum
1«m8 weekly) Permissible intake from all sources for children
1971). Lead concentrations of 80 ug/100 ml of blood or 200 ye/1
of urine traditionally have served as biologic threshold limit values in
determining the safe" levels of occupational exposure.
5.1.2 Metabolism and Bioac cumulation
The absorption and metabolism of lead depend on a number of factors
such as particle size, physicochemical form of lead, route and extent of'
exposure, as well as several other factors, such as age and nutritional
S tclCUS •
5.1.2.1 Absorption
inh .AJforPtion °f lead can occur through three exposure routes: oral,
inhalation, and dermal. In adults, uptake of lead from the gastrointes-
1974) trintvi^8e%f^°m 5 V°% °f ±ntake (Keh°e 1961< Kabinowitz et al.
1974 . In vitro studies with rats indicate lead crosses the intestinal"
barrier by a passive diffusion process linked to some degree to the
concomitant movement of water (Coleman et al. 1978). Kehoe (1961) con-
ducted an extensive series of balance studies in human volunteers for
periods ranging from several months to nine years. He found that intake
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blood lead concentration. A total dose of 1.3 mg/lead/day, however,
resulted in a progressive increase in urinary excretion of lead and in
the lead content of blood and other tissues. Goyer and Mushak (1977)
estimate that every 100 milligrams of dietary lead contributes about
10(6.4-15) milligrams of blood lead per 100 milliliters in adults.
More recently, attention has been focused on the increased absorption
of dietary lead by infants and young children (Alexander et_ al. 1973.
Roels et al. 1978, McCabe 1979). Alexander and co-workers (1973) reported
increased absorption of lead (53%) from the gastrointestinal tract in eight
normal children between the ages of 3 months and 8 years, although they
examined a small amount of children. Similarly high absorption rates have
been noted in young experimental animals (Rosen and Sorell 1978
Momcilovic 1978, 1979).
Animal studies have also revealed several dietary factors that can
influence gastrointestinal absorption. Two critical nutritional require-
ments for a growing mammal are the supply of calcium for bone growth and
the supply of iron for red blood cell production. A reduction of either
calcium or iron in the diet can result in an enhanced absorption of lead
(Granick et al. 1978, Six and Goyer 1972). Iron deficiency in infants
may also result in pica and, thus, predispose children to increased lead
exposure. Other factors, such as high intake of dietary fat, deficiencies
of^certain vitamins and minerals, ethanol ingestion, stress, strain of
animal, etc., can affect absorption and the resulting toxicity of lead in
experimental animals (Barton and Conrad 1978, Bushnell et al. 1979
Levander 1979, McCabe 1979, Mykkanen et al. 1980).
Studies in humans indicate that 30+10% of lead inhaled is deposited
in the lungs (WHO 1977, Tsuchiya 1979) and that the amount of lead
retained will vary considerably depending on the size of the particle
and the depth and frequency of respiration. There is no evidence that
lead accumulates in the lungs or that all lead retained is eventually
absorbed or transferred to the gastrointestinal tract (Tsuchiya 1979).
An indirect but useful measure of lead deposition and retention in the
airways can be made from blood lead levels. A general consensus is that
an air lead level of 1 yg Pb/mJ will increase blood lead concentrations
in adults by approximately 1 ug Pb/100 ml whole blood (Mahaffey 1977,
WHO 1977). Such a relationship has not been defined for children.
Absorption through the skin is only important in the case of organic
compounds of lead; because of their lipid-solubility, organic lead com-
pounds penetrate skin to a significant degree (Barry 1978). Inorganic
lead salts do not readily penetrate intact skin. In an experiment that
involved the application of lead acetate to the foreheads of eight male
volunteers, Moore and co-workers (1980) discovered that between 0 and
0.3% of the dose was absorbed.
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5.1.2.2 Distribution and Retention
Absorbed lead is transported by blood and initially distributed
according to blood distribution patterns; subsequently, it is redis-
tributed to various compartments. Under conditions of continuous intake
over a prolonged period of time, a near steady state is achieved with
respect to intercompartmental distribution. The kinetics of lead
distribution and accumulation in humans have not been well defined.
Rablnowitz and co-workers (1976), however, have examined the distribution
of lead (^4pb) under dynamic conditions in five healthy men. The data
obtained could be explained on the basis of a three-compartment model.
The first pool, blood, contains 1.7-2.0 milligrams lead with a lifetime
of 27-40 (mean 35) days. The second pool consists mainly of soft tissues
It contains 0.3-0.9 milligrams lead and has a lifetime of 30-55 days. The
third pool, composed of hard tissues (mainly skeleton), contains most of
the body burden of lead.
The accumulation of lead begins during fetal life. Lead is readily
transferred across the placenta and has been detected in the human fetus
as early as 12-14 weeks of gestation (Rosen and Sorell 1978). Among
normal individuals, the total body burden of lead increases from approxi-
mately 0.2 mg at birth to values up to 200 mg during a person's lifetime;
this increase is limited almost entirely to an increasing storage of lead
in the calcified matrix of the bone (Chisolm and Barltrop 1979). Barry
(1975, 1978) estimates the total lead content of the body may reach
119 mg in women, 165 mg in men without occupational exposure to lead,
and 522 mg in men with occupational lead exposure.
The concentration of lead in blood (PbB) is of prime importance in
the determination of recent lead exposure. Lead circulating in the blood
is principally (-90%) bound in a slow diffusable form in the erythrocytes;
the remainder, the diffusable fraction, is in the plasma (Butt et_ al.
1964, Posner 1977). Recent data suggest that most adult populations in
the United States have mean PbB of about 10-20 yg/100 ml; approximately
3.5% of the adult population may have levels above 30 yg/100 ml (NRC 1980).
Lead levels in erythrocyte and plasma of 75 pregnant women and their
infants at delivery were measured by Cavalleri and co-workers (1978). No
significant differences were found in maternal and fetal values. The mean
lead erythrocyte concentrations were 26.4 and 25.4 yg/100 ml in mothers
and newborns, respectively. Plasma values were 0.66 and 0.62 yg/100 ml,
respectively. Similar PbB values were noted in 500 Belgian mothers and
their newborn infants (Roels .ejt .al. 1978).
Robinson and co-workers (1958) reported PbB values of 7-28 yg/100 ml
in 9 neonates, 5-31 (median 15) yg/100 ml in 28 infants up to 6 months of
age, and 3-54 (median 27) yg/100 ml in 75 children from 6 months to 13
years in age. In adults, normal PbB values range from 5-40 yg/100 ml
(Goldwater and Hoover 1967) with no significant difference in PbB values
of smokers (19.9 yg/100 ml) and nonsmokers (19.0 yg/100 ml) (McLaughlin
and Stopps 1973).
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Of 176 children between the ages of one to 9 years living within 20
miles or a lead smelter in Idaho, Walter et al. (1980) discovered that
174 had PbB levels exceeding 40 ug/100 ml; 105 of these children had
PbB values >60 yg/100 ail. In contrast, Baker et al. (1977) reported
PbB levels within normal limits in children living within 3 kilometers
of a lead smelter.
Lead also concentrates in the teeth, particularly in secondary
dentine; however, it appears to be firmly bound and unavailable for
release. At present, there is no general consensus on what constitutes
a normal or acceptable level of lead in teeth (Barry 1978).
5.1.2.3 Elimination
About 90% of ingested lead is eliminated, unabsorbed, via the feces
(Kehoe 1961). Absorbed lead is principally excreted via the urine (7670
with lesser amounts in gastrointestinal secretions (16%) and miscellaneous
routes of excretion, such as breast milk, sweat, exfoliated skin, hair,
and nails (8%) (Rabinowitz ej: al. 1973). Normal levels of lead in urine
are in the 30-40 yg/100 ml range (McLaughlin and Stoops 1973, Rabinowitz
_et al. 1973). Human breast milk contains < 5-12 jg/i (Hammond 1977).
5.1.2.4 Metabolism of Organolead Compounds
Organolead compounds, i.e., tetraethyllead and tetramethyllead, are
readily absorbed from the gastrointestinal tract, lungs, and skin (Cohen
1979). They are dealkylated to trialkyl lead compounds by mixed function
oxidases in the liver (Bolanowska 1968, Grandjean and Nielsen 1979). The
trialkyl form accumulates in nonosseous tissues, particularly the liver,
kidney, and brain. In rats, the half-life in liver and kidney is
approximately 40 days for trimethyllead and 15 days for triethyllead
(Hayakawa 1972). Tetramethyllead is also absorbed through skin and
dealkylated to the trialkyl form more slowly than tetraethyllead
(Grandjean and Nielsen 1979, Cremer 1965).
In a study of twenty-two individuals living in the vicinity of
Copenhagen, Nielsen et al. (1979) reported a median concentration of
0.014 yg trialkyllead/g brain tissue in these individuals who had no
occupational exposure to organic lead. This quantity accounted for
approximately 20% of the total lead content of the brain.
5.1.3 Human and Animal Studies
In many respects, the toxic effects associated with lead exposure
are similar in both experimental animals and humans. Therefore, where
considerable human data are available, the primary focus was placed on
humans and more specifically on data that are most useful in the assess-
ment of acceptable limits of human exposure to lead. In areas of scant
or nonexistent human data, supplemental animal data are presented in
detail.
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5.1.3.1 Carcinogenesis
Animal Data
Oral or parenteral administration of rather high doses of some lead
salts have produced benign and malignant renal tumors in rodents. How-
ever, lead toxicosis and high mortality were also associated with these
studies. Zollinger (1953) was the first to observe renal tumors following
long-term subcutaneous injection of rats with lead phosphate; 19 of 29
rats (65.5%) that survived treatment for longer than 10 months developed
renal tumors. Total doses ranged between 120 and 680 milligrams of lead.
More recently, lead-induced renal tumors have been confirmed in
both rats and mice fed diets containing 0.1 and 1% basic lead acetate
(Van Esch and Kroes 1969, Oyasu _et al. 1970, Van Esch .et al. 1962, Mao
and Molnar 1967) and in rats fed 1% lead acetate (Boyland et al. 1962
Goyer and Rhyne 1973). '
In addition to renal neoplasms, Zawirska and Medras (1968) observed
tumors of the testes, adrenals, thyroid, pituitary and prostrate glands
in rats fed diets containing lead acetate (3 mg/rat/day for 2 months; 4
Img/rat/day for 16 months. Oyasu _e_t _al. (1970) reported gliomas (11.8%
versus 0.3% in controls) as well as renal tumors (76%) in male Sprague-
Dawley rats fed 1% basic lead acetate in the diet for approximately one year,
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Renal changes but no neoplasms were found in male hamsters fed
0.1 or 0.5% basic lead acetate for two years (Van Esch and Kroes 1969)
and in male rats fed diets containing 0.1% lead arsenate or 0.1% lead
carbonate for two years (Fairhall and Miller 1941).
Co-carcinogenic activity of lead salts has been demonstrated in rats
and hamsters. Hinton and co-workers (1979) observed a co-carcinogenic
interaction between lead and FBPA (N-[4'-fluoro-4-biphenyl] acetamide)
resulting in the development of renal adenocarcinoma in rats. This was
demonstrated by decreasing the latency period, increasing the tumor
yield, and increasing the percentage of tumor-bearing rats. However,
similar results were not observed in the liver, in fact the addition'of
1% lead (as lead acetate) to the FBPA-diet provided early protection
from the onset as well as retardation of later development of hepato-
cellular carcinoma.
In another study, intratracheal administration of 1 mg lead oxide
with 1 mg benzo(a)pyrene per week for 10 weeks resulted in lung adenomas
in 11 of 26 (42%) Syrian hamsters within 60 weeks. One adenocarcinoma
of the lung was also observed. These tumors were not noted in hamsters
given the same dose of either lead oxide or benzo(a)pyrene alone
(Kobayashi and Okamota 1974).
A single carcinogenicity study with organic lead noted that sub-
cutaneous injection of 0.6 milligrams of tetraethyllead given as 4
equally divided doses to Swiss mice between birth and 21 days of age
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resulted in malignant lymphomas in 1 of 26 males and 5 of 41 females
between 36 and 51 weeks. The incidence of this lesion in controls was
1 of 39 in males and 0 of 48 in females (Epstein and Mantel 1968). The
significance of this finding, however, is difficult to assess because
lymphomas occur spontaneously in this strain of mice.
Observations in Humans
Although human data are scant, no evidence suggests that lead is
carcinogenic to humans (IARC 1972). In a study of 425 former employees
of an accumulator factory, Dingwall-Fordyce and Lane (1963) found no
evidence of an elevated incidence of malignant neoplasms. A significant
excess number of deaths was noted in 170 workers with high lead exposures
(100-250 yg/lead/100 ml urine) over the past 20 years; however, mortality
predominantly resulted from vascular lesions of the central nervous
system rather than neoplasia.
In another study, no suggestion of a relationship between lead
exposure and death from cancer was found in 442 orchardists who at one
time sprayed fruit trees with lead arsenate (Nelson ^t al^. 1973).
In more recent studies (Cooper and Gaffey 1975, Cooper 1978), no
consistent association between the incidence of cancer deaths and either
length of employment or estimated lead exposure could be found in a
cohort of 7032 heavily-exposed workers employed for more than one year
from 1946-70 as smelter or lead battery workers (67% PbB 2. 40 yg/100 ml,
20% 2. 70 ug/100 ml). Further study of an additional 491 deaths in the
same population during the period 1970-75 also resulted in no correlation
between lead exposure and incidence of cancer (Cooper 1980).
With respect to organolead, a single report by Robinson (1974) noted
no increased cancer rate in a 20-year follow-up of 592 workers exposed
to tetraethyllead. A 20-year latency period, however, is insufficient
to exclude carcinogenicity and may well underestimate the true incidence
of cancer..
Thus, experiments with small rodents indicate that the addition of
0.1 or 1% basic lead acetate to the diet of rats and mice or 1% lead
acetate to the diet of rats is carcinogenic, resulting in an elevated
incidence of renal tumors. An increased frequency of adrenal, thyroid,
brain, pituitary, and prostate tumors has also been associated with
exposure of rats to lead acetate; however, these data require confirma-
tion. Lead salts have also been shown to exhibit co-carcinogenic
activity in rats and hamsters. No indication of tumors was reported
following exposure to lead carbonate or lead arsenate; however, this
evidence cannot be held as conclusive. Although human data are scant,
no evidence suggests that lead is carcinogenic in humans. The equivalent
human dose to dietary levels producing renal tumors in laboratory animals
is 550 mg/day elemental lead (IARC 1972), which is far in excess of the
maximum tolerated dose of lead for humans.
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5.1.3.2 Mutagenesis
The evidence on a possible association of lead exposure and chromo-
somal aberrations in humans is inconclusive and contradictory. Chromo-
somal aberrations have been reported in some workers in lead industries
(Deknudt et al. 1973, Bauchinger _et al. 1976). These studies, however,
involved mixed exposures (Pb, Zn, Cd), which may be a contributing
factor to the positive findings. However, an increased frequency of
aberrations has been reported in in vitro studies with human lymphocytes
exposed to lead acetate (10~*-lCrb M) in culture (Schwanitz et al. 1970
Beek and Obe 1974, Obe _et _al. 1975).
Numerous other observations have essentially been negative.
O'Riordan and Evans (1974) found no significant increase in chromosomal
aberrations in shipbreakers exposed to lead oxide fumes; the study
population had PbB values ranging from 40 pg to >120 ug/100 ml.
Bauchinger and co-workers (1972) found no abnormalities in the chromo-
somes of policemen with PbB levels elevated 20-30% above control values.
Deknudt et al. (1977) noted a random increase in the incidence of rings
and dicentric chromosomal aberrations in lymphocytes of some smelting
plant workers; however, no correlation could be established between the
number of aberrations and PbB, age, or length of exposure. PbB values
ranged from 44 ug to 95 yg/100 ml. Negative results were also noted in
human lymphocytes exposed in culture to 10-6-10-2 M lead acetate (Schmid
.et al. 1972).
Thus, whether exposure to lead can induce chromosomal abnormalities
in humans remains an unanswered question because of the lack of sufficient
data on the issue.
Data from animal studies are also conflicting. Muro and Goyer
(1969) noted that chromosomes from bone marrow cells of mice fed 1% lead
acetate in the diet for two weeks showed an increased number of chromatid
aberrations (gaps and fragments). These aberrations involved single
chromatids, which suggest that injury followed DNA replication and thus
could have been produced in culture. However, mice exposed to 1800 mg
lead acetate/liter in drinking water for one year exhibited no increased
chromosomal aberrations in either spermatocytes or marrow cells (Leonard
et al. 1973) and no increase in aberrations was noted in Chinese hamster
cells exposed in vitro to various concentrations of lead acetate
(Bauchinger and Schmid 1972).
DiPaolo and co-workers (1978) noted that relatively high concentra-
tions of lead acetate enhanced transformation of Syrian hamster cells by
a simian adeno-virus (SA7) in vitro. Enhancement ratios of 3.1, 1.9,
1.4, 1.55, and 1.0 were recorded for hamster embryo cells exposed for
18 hours in culture to 200, 100, 50, 25, or 0 yg/ml lead acetate,
respectively. Subcutaneous injection of transformed cells into either
Syrian hamsters or nude mice produced fibrosarcomas.
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With respect to organic lead, negative findings were reported in a
dominant lethal study with tetraethyllead in mice (Kennedy et al. 1975).
while exposure of Drosophila melangoster to this compound resulted in an
increased occurrence of nondisjunction and chromatid breaks (Ahlbers
et al. 1972, Ramel 1973).
In summary, the available experimental data do not provide unequivo-
cal proof of the mutagenic activity of lead. Results are often conflicting
and do not allow a satisfactory evaluation of the genetic risks of lead.
5.1.3.3 Adverse Reproductive Effects
Animal Data
Several animal studies indicate that sublethal lead exposures may
impair normal reproductive ability. Impotence and prostate hyperplasia
were observed in sexually mature male rats exposed to lead acetate for
30 days; blood lead levels were 14-26 yg/100 ml. Testicular damage with
inhibition of spermatogenesis occurred in rats with PbB of 50-100 yg/100
ml. Similarly exposed female rats exhibited irregularities of the estrus
cycle at PbB 14-30 yg/100 ml. Ovarian follicular cysts developed in
females when PbB reached 50 yg/100 ml (Hilderbrand et al. 1973). A sub-
sequent study (Der et_ al. 1974), however, was unable to replicate these
findings in Sprague-Dawley rats.
In another study, Krasovskii and co-workers (1979) noted decreased
sperm mobility and increased acid phosphatase activity in the gonadal
tissue of rats fed 50 yg lead/kg (as lead acetate) daily for 20-30 days.
Small disruptions in the permeability of vessels and dystrophic changes
in the Leydig cells were also reported. No effects were seen in another
group of rats identically treated with 1.5 yg lead/kg/day.
Similarly, Balb/c male mice fed 0.1% lead acetate in the diet for
16 months exhibited no impairment of fertility, which was judged by
their ability to impregnate untreated females. The incidence of abnormal
sperm in these treated mice was comparable with control values. A second
group of mice fed 1% lead acetate in the diet exhibited, within 8 weeks,
a doubling in the mean number of abnormal sperm compared with controls.
However, no consistently significant reduction in sperm count or sperm
motility was seen. Unfortunately, males at this treatment level were
not mated with virgin females to establish the effect on fertility
(Eyden .et al. 1978).
Sexual maturation also appears to be disrupted by lead exposure.
Kimmel .e_t .al. (1976) reported a dose-related delay in puberty (vaginal
opening) in female rats exposed from conception to 25, 50, or 250 mg/1
lead acetate in drinking water, which, at least for the lowest dosage
group, was not secondary to reduced body weight. In a later study
utilizing the same treatment regimen, Kimmel et al. (1980) indicated
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that delayed puberty did not affect the ability to conceive, to carry a
normal litter to term, or to deliver the young. No significant increases
in resorptions, malformations, or postnatal deaths were produced. Gray
and Reiter (1977) noted a similar delay in female mice administered 5 mg
lead/ml in drinking water at parturition; no delay in vaginal opening was
noted in pair-fed control mice.
In pregnant animals, large amounts of lead can prevent implantation
and cause embryonic death. In addition, a few studies have demonstrated
a^teratogenic effect following an acute dose of lead, although malforma-
tions have not been observed in most experimental investigations.
Gale (1978) observed a variable embryotoxic response to lead in
different strains of hamsters. Lead nitrate (50 mg/kg) was injected
intravenously to five inbred strains (MHA, LSH, LHC, CB, and PDA) and
one outbred strain (LVG) of pregnant hamsters early on the eighth day
of gestation. The MHA and CB strains were relatively resistant to lead
exposure; however, the other strains exhibited increased resorptions
(80-92%), tail bud abnormalities, hydrocephalus, and skeletal defects.
In rats, intravenous injection of aqueous solutions of 0, 5, or
25 mg 210pb(N03)2/kg on day 9 of gestation produced no effects at the
low dose, but resulted in 43.5% resorption and 17.7% incidence of
stunting and external malformations in fetuses in the 25 mg/kg group
examined on day 20. Dams similarly injected on day 15 of gesfcation
exhibited no overt toxicity at the low dose, but 100% resorption
occurred at the 25-mg/kg level. Injection of 25 mg/kg on day 15 was
associated with petechial hemorrhages in fetal brain within 90 minutes
of dosing with more massive hemorrhaging consistently noted 24 hours
post-dosing (Hackett _e_t al. 1978).
Gerber and co-workers (1978) noted pregnant C57B1 mice fed diets
containing 0.5 or 0.25% lead (as lead acetate) exhibited decreased
pregnancy incidence, increased embryonic death, and retarded growth in
surviving embryos. Maisin et al. (1975) noted similar findings in mice
fed 0.1 or 0.5% lead in the diet during gestation. In contrast, Kennedy
et al. (1975) reported no effects on the number of fetuses resorbed, the
number of viable fetuses, or the incidence of terata in either mice or
rats. In this study, 7.14, 71.4, or 714 mg/lead/kg was administered to
mice and rats on days 5-15 and days 6-16 of gestation, respectively.
Urorectocaudal malformations were produced in the surviving offspring
of rats injected intravenously with 50 mg lead nitrate/kg on day 9 of
gestation. Malformations noted include absence of tail (21%), absence of
genitalia (23%), imperforate anus (12%), and sirenomelia (16%). None of
these abnormalities was present in untreated controls. These malforma-
tions were not observed in rats injected with the same dose on day 16 of
gestation; however 40% of survivors were hydrocephalic (McClain and
Becker 1975). Tail abnormalities, ranging from stunting to the' complete
absence of the tail, have been reported in hamsters following injection
of dams with various lead salts (Ferm and Carpenter 1967). In addition,
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treatment of chick embryos with lead salts has been shown to produce
hydrocephalus and meningoceles (Butt &t al. 1952, Mclaughlin et al.
1963), as well as cardiac abnormalities (Gilani 1973).
_ With respect to organic lead, the inability of the fetus to metabo-
lize tetraelkyllead compounds to their trialkylform appears to protect
the fetus. No terata have been observed in either rats (Odenbro and
Kihlstrom 1977, Kennedy et al. 1975) or mice (Kennedy et al. 1975)
exposed in utero to tetralead compounds. Increased resorption of fetuses
growth retardation, and incomplete bone ossification were noted in rats
exposed to either tetraethyl- or tetramethyl-lead; however, these inci-
dences occurred only as a result of doses that produced distinct maternal
toxicity (McClain and Becker 1975).
Observations in Humans
Lead exerts a profound, adverse effect on the fetus and interferes
with the reproductive ability of both men and women at PbB levels of
30-40 ug/100 ml (NRC 1980). Several stages of the reproductive process
are vulnerable to lead. They are the sperm and/or egg prior to concep-
tion, the embryo during pregnancy, and the neonate.
Historically, lead exposure has been linked to disturbances of
menstruation and elevated incidences of miscarriages and stillbirths in
women working in lead industries. This was particularly the case during
the latter half of the 19th century. Recently, Panova (1972) reported
that women working in a printing plant for 1-12 months at ambient air
levels of < 7 yg Pb/m3 had a higher incidence of ovulatory dysfunction
(mainly anovulatory cycles) compared with a control group. In a critical
review of this study, however, Zielhuis and Wibowo (1977) noted the
difficulty in evaluating Panova's conclusions because of the design of
and the presentation of data. More importantly, no consideration appears
to have been given to the dust levels of lead, which is an important
consideration in print shops.
Lead absorbed into the bloodstream of pregnant women crosses the
placenta and enters the blood of the fetus. Umbilical cord blood lead
levels are similar to those found in mother's blood (Cavalleri et al.
1978). Because the fetus develops rapidly, it is particularly vulnerable
to intrauterine exposure to lead. Furthermore, calcium and iron defici-
encies, which are commonly observed in pregnant women, cause the mother
to have a higher risk of lead toxicosis.
Both Lane (1949) and Nogaki (1958) suggest that miscarriages can
occur in women with only modest exposure to lead; and Wibberley _et al.
(1977) recently noted a striking increase in the level of placentaYTead
associated with stillbirths. Fahim et al. (1976) reported elevated
incidences of pre-term deliveries (13 versus 3 in controls) and early
fetal membrane rupture (17 versus 0.41 in controls) in women living in
a lead mining area of Missouri compared with women living in an urban
environment in Missouri. One confusing aspect of this study, however, is
the unexplained similarity in PbB levels in all mothers,
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There are also reports on the effects of lead on the male reproduc-
tive function. Lancranjan _et al. (1975) reported evidence of decreased
fertility in occupationally-exposed men. These disturbances included
alterations in spermatogenesis (increased frequency of asthenospermia,
hypospermia and teratospermia) in men with PbB of 50-80 yg/100 ml. No
effects were noted in the 23-41 yg/100 ml PbB range. Reduced sexual
potency, testicular pain, and a reduced number of spermatozoa have been
reported in workers exposed to tetraethyllead (Vurdelja et al. 1967
Neshkov 1971).
No data suggest that lead is teratogenic in humans. One report
(Palmisano ej: al. 1969) suggested a possible link between maternal
consumption of lead-contaminated whiskey with neuromuscular abnormali-
ties and failure to thrive in a ten-week-old infant whose mother
had lead poisoning concomitant with alcoholism.
Thus, several studies indicate that exposure to high levels of lead
may impair normal reproductive ability in experimental animals (e.g.,
testicular damage, irregularities of the estrus cycle, disruption of
sexual maturation). In pregnant animals, lead is embryotoxic; and, at
least in some species, lead induces terata of the urorectocaudal region
subsequent to acute lead exposure. A number of investigators, however,
have observed no increase in the incidence of terata in experimental
animals exposed to lead during gestation.
Lead also exerts significant adverse effects on the reproductive
function in humans; however, most available data are related to high
occupational exposure and therefore are difficult to extrapolate to
normal exposure levels. No evidence suggests that lead is teratogenic
in humans.
5.1.3.4 Other Toxic Effects
No beneficial effects of lead have been found. Because of its
accumulation in bone tissue, even a low daily intake of lead can even-
tually produce toxic effects. Although other systems may be adversely
affected, in humans, as in experimental animals, the three principal
target organs for lead are the erythroid cells of the bone marrow, the
kidney, and the central and peripheral nervous systems. The inhibitory
effects of lead on erythropoiesis are reversible; however, severe acute
or chronic lead poisoning may be followed by irreversible injury to the
kidney and nervous system.
Hematopoietic System
Exposure to lead results in derangement of the hematopoietic system
with disruption of hemoglobin synthesis considered the critical or first
adverse effect of lead exposure. Lead interferes with hemoglobin syn-
thesis at a number of steps: (1) it causes partial inhibition of several
enzymatic steps in the biosynthesis of heme; (2) it impairs the uptake
and use of iron; and (3) it impairs globin synthesis in the developing
erythroid cells of the bone marrow.
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Heme is formed in the mitochondria and is an essential component
of the cytochrome system and cell respiration. Heme also serves as the
prosthetic group of hemoglobin, the protein that transports oxygen from
the respiratory system to the cells of the body. The biosynthesis of
heme is a multi-step process. At least two of these steps are considered
directly inhibited by lead. These are: (1) the transformation of
5-aminolevulinic acid (ALA) into porphobilinogen, catalyzed by <5-amino-
levulinate dehydratase (ALAD); and (2) the insertion of iron in proto-
porphyrin IX to form heme, catalyzed by ferrochelatase (heme synthetase)
(Hammond 1977, Chisolm 1978). Lead also affects other steps in the
process of heme synthesis, such as 6-ALA synthetase and coprogenase.
However, these effects may be secondary results of feedback derepression
rather than a direct effect of lead (Hammond 1977).
Although specific inhibition of ferrochelatase by lead is generally
accepted as the cause of the accumulation of protoporphyrin in the
erythrocytes, lead probably also inhibits the availability of iron for
coupling with protoporphyrin (WHO 1977). Globin synthesis in the red
blood cells is also apparently impaired; however, the mechanisms that
cause reduced globin synthesis are unknown (WHO 1977).
In general, clinical anemia does not occur until PbB levels are
>80 yg/100 ml (Muir and Bridbord 1977). The available data (Tola et _al.
1973) suggest, however, that mild anemia with a small reduction in blood
hemoglobin may occur in adults at or slightly above the dose levels
associated with a minimal increase in urinary excretion of ALA (PbB
50 ug/100 ml. Children appear to be more sensitive to lead anemia than
adults; reduction in hemoglobin may occur at PbB of -40 yg/100 ml (WHO
1977). An increased rate of erythrocyte breakdown (decreased erythrocyte
life) is often, but not consistently, seen in cases of anemia as a result
of lead poisoning (WHO 1977).
Indicators of the critical effect of lead on hemoglobin synthesis
include rapid depression of ALAD activity, an associated increase in
urinary ALA, and a delayed rise in free erythrocyte protoporphyrin (FEP)
in blood (Chisolm 1978).
Because'lead acts directly on the circulating erythrocytes, the
rapid depression of ALAD activity most closely correlates with the
concentration of lead in the blood. There is an inverse linear rela-
tionship between the logarithm of ALAD activity in erythrocytes and the
concentration of lead in whole blood over a PbB range of 5-95 yg/100 ml.
The average no-effects PbB threshold for inhibition of erythrocyte ALAD
activity is about 10-20 yg/100 ml (Tola et al. 1973). Nordman and
Hernberg (1975), however, have reported an inhibition of ALAD at PbB
of 8.4 yg/100 ml, which raises questions concerning the existence of
a no-effect level. The toxicological implications of ALAD inhibition
are not adequately known.
Significant inhibition of ALAD is associated with the accumulation
and excretion of excess ALA in urine and a rise in blood FEP. The
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relationship between ALA in urine and PbB is not linear; the increase
of ALA in urine becomes marked when PbB is >40-60 yg (Tsuchiya 1979).
The rise in FEP and the depression of ALAD activity are almost equally
as sensitive as indices of lead exposure. FEP elevation is delayed
by approximately two weeks because it reflects inhibitory effects
occurring in erythroid cells in the bone marrow (Hammond 1977). Women
and children appear to have an earlier and more rapid increase in FEP
than men for the same levels of PbB. Blood lead threshold for the FEP
response is -15-20 ug/100 ml for adult females and children and -25-30
yg/100 ml for adult males (Zielhuis 1975). The reasons for these
differences are not entirely clear; however, they may be related to
differences in iron stores, hormonal factors, and growth rate (Roels
.et al. 1978).
Renal System
The nephropathic effects of lead intoxication are profound. Two
stages of lead-induced nephropathy are: (1) proximal tubular morpho-
logic changes accompanied by a reversible tubular dysfunction, which is
seen mainly with short-term exposure; and (2) interstitial fibrosis,
which is generally considered to be of a slow, progressive nature and
which eventually causes contracted kidneys and chronic renal failure
(Goyer 1979, Payne and Saunders 1978).
Acute lead nephropathy in children is characterized by dysfunction
of the proximal renal tubules (Fanconi's syndrome) manifested as glyco-
suria, hypophosphatemia with phosphaturia and generalized aminoaciduria
(Granick _et al. 1978). Pueschel et al. (1972) reported generalized
aminoaciduria in 8 of 43 children with PbBs of 40-120 ug/100 ml and
slight lead-related neurological signs. Similar symptoms have been
observed in occupationally-exposed adults (Clarkson and Kench 1956,
Goyer ejt al. 1972); however, PbB levels were not reported. In adults,
amonoaciduria is probably uncommon at PbB levels <70 ug/100 ml (U.S. EPA
1980). Changes in the proximal tubules include the formulation of
intranuclear inclusion bodies of lead-protein complexes and alterations
in mitochondrial structure and function (Goyer and Mushak 1977). Treat-
ment with chelating agents will reverse a minoaciduria along with the
functional and morphological changes associated with lead toxicity
(Goyer and Mushak 1977).
It is uncertain if acute lead nephropathy, treated or untreated,
influences the development of any form of chronic nephropathy without
continuous lead exposure. An Australian study indicated that long-term
exposure to lead early in life could result in chronic nephropathy in
adulthood (Emmerson 1968). On the other hand, Tepper (1963) was unable
to find evidence of chronic nephropathy in young American adults 10-20
years after childhood lead poisoning. A recent study in rats (Fine et_ al.
1979) also reported no indications of progressive, interstitial nephro-
pathy or alterations in renal growth or development, despite an acute
increase in the body burden of lead in growing rats.
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Long-term exposure to lead may result in the development of irrever-
sible functional and morphological renal changes. The second stage of
lead nephropathy has the morphologic appearance of an interstitial
nephritis. Interstitial fibrosis becomes progressively severe with
tubular atrophy and eventually reduced glomerular filtration progressing
into renal failure (Goyer 1979).
Reduced glomerular filtration occurs at relatively low levels of
lead exposure (Weeden e_t al_. 1975, Cramer et. al. 1974, Lilis et al.
1979). Weeden and co-workers (1975) reported reduced glomerular filtra-
tion rates in four of eight men occupationally exposed to lead (PbB
48-98 yg/100 ml). Lilis et al. (1979) noted a sizable reduction in the
glomerular filtration rate (age-adjusted) of 255 secondary lead smelting
workers. A significant increase in blood-urea-nitrogen and serum
creatinine levels, which correlated with the duration of lead exposure,
were also documented. A total of 18, 37, 37, and 77, of the test popula-
tion had PbB levels in the >80, 60-79, 40-59 and <40 yg/100 ml,
respectively.
Thus, proximal tubular dysfunction can occur in both children and
adults and are generally noted after short-term exposure. Kidney disease
associated with chronic lead exposure has not been adequately studied and
is difficult to detect, i.e., blood urea nitrogen and serum creatinine
become elevated only when two-thirds of the kidney function is lost.
Little is known about dose-response relationships; however PbB >70 pg/100
ml for a prolonged period are believed to give rise to chronic irrever-
sible nephropathy (Goyer 1979).
Central and Peripheral Nervous Systems
Among the most devastating effects of increased lead absorption are
the effects on the central and peripheral nervous systems. Toxic levels
of lead in the central nervous system (CNS) can interfere with neuro-
transmitters or the levels of essential metals as well as inhibit various
enzyme systems, some of which are responsible for the energy metabolism
of the brain (Granick e_t al. 1978). Manifested as encephalopathy,
effects on the CNS are seen more frequently in children than adults.
This may be attributed to several factors; e.g., children absorb more
lead from the diet than adults; the brain is especially vulnerable to
insult during the period of rapid neurodevelopment; and behavioral
patterns, such as pica, may predispose children to higher lead exposure.
In addition to age, the severity of encephalopathy also depends on the
intensity and duration of exposure. Major features of encephalopathy
are: dullness, hyperkinetic or aggressive behavior, headaches, muscular
tremors, hallucinations, and, in severe cases, convulsions, mania,
paralysis, and coma (WHO 1977). The minimal level of lead exposure
associated with lead encephalopathy in children is not clearly known;
however, it is estimated to be 80 ug/100 ml PbB (WHO 1977).
Arnvig and co-workers (1980) reported that nine men with occupa-
tional exposure to lead in a battery plant exhibited PbB levels of
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58-82 yg/100 ml. The authors conducted numerous psychological tests on
these men and observed severe deficiencies in memory tests, concentration
and attention, and psychomotor performance. Although they did not evalu-
ate a control group, the authors feel that serious abnormalities were
identified.
Recently, however, several studies have raised questions about the
subtle impairment of the cerebral function in children at sub-encephalo-
pathic blood lead levels (40-80 yg/100 ml) (Landrigan et_ al.. 1975,
De la Burde and Choate 1972, 1975, Perino and Ernhart 1974). These
studies, however, have been subject to criticism because of flaws in
the experimental design, such as overlapping of lead exposures between
test and control populations, insensitivity of behavioral tests, compli-
cations of nutritional and socioeconomic status, etc. General findings
of a few key studies are discussed below; however, the interested reader
is urged to review the detailed analyses of the neurological and behav-
ioral effects of lead by Repko and Corum (1979), Needleman (1980),
and the U.S. EPA (1977).
De la Burde and Choate (1972, 1975) compared children with a history
of pica and elevated PbB (>40 yg/100 ml) with control children with no
history of pica. The lead-exposed children showed mental impairment,
irritability, and poor fine motor coordination. Although the groups were
matched for race, age, sex, and socioeconomic variables, no lead assess-
ments were made for the control group.
A controversial study by Landrigan e_t al. (1975) reported neuro-
logical dysfunction in 46 symptom-free children (3-15 years) with
moderately elevated blood lead concentrations (mean 48 ug/100 ml) when
compared with children with PbB <40 yg (mean 27 yg/100 ml). The lead-
exposed group showed lower scores (Wechsler Intelligence Scale) and
poorer results in the finger-wrist tapping test than controls. However,
no differences were exhibited between the groups in full-scale I.Q.,
verbal I.Q., or hyperactivity behavior ratings. No conclusive evidence
of lead as a causative factor was presented. . Perino and Ernhart (1974)
also concluded that neurobehavioral deficits occurred at PbB levels as
low as 40 yg/100 ml.
Diminished learning ability (I.Q. drop of 4-7 points) and behavioral
changes, such as diminished attention span in children, have also been
associated with increased concentrations of lead in teeth (Needleman
et al. 1974).
Conversely, several studies have reported negative results between
lead-exposed groups and controls (Kotok 1972, Lansdown et al. 1974,
McNeil et al. 1975). These studies, however, have the same~~type of flaws
as the studies that suggest positive correlations between low lead levels
and neurological deficits in children.
Despite problems inherent in these studies, sufficient evidence
indicates that subtle neurobehavioral effects do occur in children
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exposed to sub-encephalopathic levels of lead. The minimal level of
lead exposure, duration of exposure, and the age of susceptibility,
however, cannot be clearly defined with any degree of certainty. The
World Health Organization (1977) concluded that the probability of
noticeable brain dysfunction increases in children from PbB levels
~50 ug/100 ml.
Subtle behavioral changes have also been documented in experimental
animals (Shih and Hanin 1978, Laporte and Talbott 1978, Dietz ejt al.
1978, Bushnell and Bowman 1979). Effects noted include changes in time
perception (Dietz et. al. 1978), learning ability (Laporte and Talbott
1978, Bushnell and Bowman 1979), motor activity (Reiter et_ al. 1975),
and avoidance behavior as adults (Krigman 1978). Lin-Fu~Tl9"76)
cited several animal studies that suggest hyperactivity might result
from moderate lead exposure via mother's milk.
Hernberg ej: al. (1967) and Landrigan and Baker (1976) have also
documented the effects of lead exposure in the peripheral nervous system
of both adults and children. Peripheral neuropathy affects somatic motor
neurons and is characterized by the loss of nerve fibers (axons and
myelin sheaths) and, to some degree, segmental demyelination (Krigman
1978). Classic symptoms are wrist drop and lead "colic," a reflection
of the effect of lead on the autonomic innervation of the gut (Granick
_e_t jl. 1978). A number of studies has also documented the occurrence of
slowed nerve conduction with an approximate PbB >50 yg/100 ml (Landrigan
and Baker 1976, Hernberg ejt al. 1967, Lilis ejt _al. 1977).
5.1.4 Overview
5.1.4.1 Ambient Water Quality Criteria — Human Health
An ambient water quality criterion of 50 yg/1 lead has been estab-
lished to protect human health (U.S. EPA 1980). The criterion is based on
on calculated level that is protective of the effects of lead on heme
synthesis, the "critical effect" selected by the U.S. EPA (1980) for
establishing standards. Because children are more sensitive to the
effects of lead than adults, the U.S. EPA has established that the max-
imum safe blood lead level (PbB) for any given child should be lower
than-the threshold for a decrement in hemoglobin (PbB » 40 ug/100 ml).
The Center for Disease Control and the American Academy of Pediatrics
recommended a PbB of 30 yg/100 ml. However, the U.S. EPA (1980) has
estimated that if the geometric mean PbB was kept at 15 yg/100 ml, 99.5%
of all children would have PbB <. 30 yg/100 ml.
Non-air sources contributing to PbB levels have been estimated to
be 10-12 yg/100 ml. It is believed that dietary intake is the main
contributor to this PbB level (U.S. EPA 1980). U.S. EPA (1980) assumed
that food and the available drinking water ( ±10 yg Pb/1) are the princi-
pal contributors to a PbB level of 12 yg/100 ml, and calculated that the
consistent consumption of drinking water at the present lead standard
(50 yg Pb/1) would contribute an additional 3.4 yg/100 ml to PbB levels.
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This would yield a PbB of 15.4 ug/100 ml, attributable to food and
drinking water. A value approximately the same as the maximum geometric
mean PbB value that would maintain 99.5% of the children in the United
States at a PbB level <30 yg/100 ml. However, this blood level (15.4
Ug/100 ml) does not take into consideration contributions from air.
5.1.4.2 Other Considerations
Lead has no natural or beneficial function in the body and even a
low daily intake of lead can eventually produce toxic effects. Children
appear to be particularly susceptible to the effects of lead, which
probably reflects the marked difference in lead absorption between
children and adults. In general, young children absorb 3-10 times more
lead than adults. Between 5 and 10% of ingested lead and 30% of inhaled
lead are absorbed by an adult. Lead salts do not readily penetrate
intact skin.
Absorbed lead is transported by the blood; and, under steady-state
conditions, is believed to be distributed into three compartments:
blood, soft tissues, and the calcified matrix of bone. The concentra-
tion of lead in blood (PbB) is of prime importance in the determination
of recent lead exposure. Most adults in the United States have mean
PbB of 10-20 ug/100 ml. Approximately 90% of the lead body burden is
stored in bone. The effects of lead, however, are more closely related
to the concentration of lead in critical tissues, such as the brain and
the kidney. Although other systems may be adversely affected, the most
prominent effects of lead are noted in the erythropoietic system, the
nervous system, and in the kidney.
Lead exposure results in derangement of the heme-hematopoietic
system, with disruption of hemoglobin synthesis being the first observed
adverse effect of lead exposure. In general, clinical anemia does not
occur until PbB values are >80 ug/100 ml; however, mild anemia may occur
with PbB levels of ~40 ug/100 ml in children and at or slightly above
50 ug/100 ml in adults.
The effects of lead exposure on the central and peripheral nervous
systems include encephalopathy, interference of neurotransmitters, and
inhibition of various enzyme systems responsible for energy metabolism
in the brain. Encephalopathy is rare in adults but more frequent in
children. The lowest reported PbB effect levels are 80 ug/100 ml for
children and 100 ug/100 ml for adults. Recently, subtle neuro-behavioral
impairments have been reported at PbB levels for which no overt symptoms
of lead toxicity are seen. Although data are somewhat contradictory,
the evidence suggests a slight cognitive impairment and possible behav-
ioral effects in individuals with PbB concentrations persistently greater
than 40 ug/100 ml. Below this value, some effects are indicated; however
the evidence, to date, is inconclusive.
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The nephropathic effects of lead intoxication are profound.
Proximal tubular dysfunction can occur in both children (PbB = 40-120
Ug/100 ml) and adults (PbB >70 ug/100 ml) and is generally noted after
short-term exposure. Prolonged exposure, resulting in PbB values
>70 ug/100 ml, may cause irreversible functional and morphological renal
changes.
Although human data on the carcinogenicity of lead are scant no
evidence suggests that lead is carcinogenic to humans. Many of the
animal studies that indicate carcinogenic activity for some lead com-
pounds are not suitable for extrapolation to humans because of the
inappropriate routes of exposure. Feeding experiments with rodents
have shown that the addition of 0.1 to 1% basic lead acetate to the
diet of rats and mice or 1% lead acetate to the diet of rats is carcino-
genic, resulting in an elevated incidence of renal tumors. Lead salts
have also been shown to be co-carcinogenic in rats and hamsters. The
equivalent human dose to dietary levels producing renal tumors in
laboratory animals is 550 mg of elemental lead/day, which is far in
excess ot the maximum tolerated dose of lead in humans. No carcinogenic
activity has been noted in occupationally-exposed persons with PbB
>40 ug/100 ml.
High occupational exposures to lead have resulted in profound
adverse effects on fetuses and have interfered with the reproductive
ability of both men and women at PbB levels of 30-40 ug/100 ml No
evidence indicates that lead is teratogenic in humans. In pregnant
animals, lead is embryotoxic and, at least in some species, induces
terata of the urorectocaudal region with doses of 50 mg/kg. Several
investigators, however, have observed no increase in the incidence of
terata in experimental animals exposed to similar levels of lead during
gestation. Exposure to high lead levels, however, does impair normal
reproductive ability in experimental animals (e.g., testicular damage,
irregularities of the estrus cycle, disruption of sexual maturation).
Evidence for a possible association of lead exposure and chromosomal
aberrations in humans is inconclusive and contradictory. Chromosomal
aberrations have been reported in some workers in lead industries; these
studies, however, involved exposures to multiple agents that may confound
reported findings. Numerous other observations have been essentially
negative. Data from animal studies are also conflicting.
Thus, a multitude of adverse health effects are associated with lead
intoxication. Blood lead levels in the 30-40 ug/100 ml range are the
lowest effect levels reported to date. Some evidence indicates adverse
effects below this value; however, to date, the evidence is inconclusive.
Therefore, the lower limits of lead exposure at which toxic effects may
occur cannot be quantified accurately.
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5.2 HUMAN EXPOSURE
5.2.1 Introduction
The effects of lead on humans have been studied for years as de-
scribed in the previous section. In order to deal with this problem
numerous regulatory mechanisms have been initiated; i.e., setting an'
air quality standard, a drinking water standard, and a limit on lead
content in paints (NRC 1980). m addition, lead screening programs
have been established for children, and some states have enacted laws
intended to deal with this hazard.
Although "undue" exposure to adults appears limited primarily to
occupational settings, exposure to lead is prevalent among children.
.
% °f 277'347 Chlldren t£Sted in the lead screening program
showed blood lead levels (PbB) >40 ug/100 ml. In 1974 and 1975 this
percentage decreased to 6.4 and 6.5, respectively. In 1976. when the
level defined as an elevated blood lead level was reduced to 30 t-e
Pb/100 ml, 8.7% of the 500,463 children screened exceeded this level
In addition, 2.7% of the children exceeded 50 yg/100 ml in the blood
?^er !r Disease Contro1 1977>- Studies of large populations of
children have shown that PbB levels show lognonnal distributions with
geometric means for city children of 20-30 pg/ml (Billick et al. undated-a
Angle and Mclntire 1979). --
One of many problems associated with the quantification of human
exposure to lead is the establishment of a background exposure. Although
a J?bB of 2:> yg/ml is not considered excessive in terms of the lead
screening program, it is probably in excess of mean PbB levels in rural
areas (Angle and Mclntire 1979) and of historical levels (Settle and
Patterson 1980). These authors have suggested that typical American
skeletal concentrations of lead are 500 times higher than ancient
Peruvian skeletons. Thus, "normal" levels of lead do not necessarily
represent acceptable levels.
An additional problem in the quantification of human exposure to
lead is that PbB is commonly used as an indication of exposure. Though
this measure can be used, to some extent, in the assessment of risk,
PbB levels indicate relatively recent exposure (Needleman et al. 1979).
Also, it is difficult to identify the source of exposure, except through
regression analyses or similar statistical methods. Although other
indices have been used to estimate exposure (i.e., hair, teeth),
especially in a relative sense, they do not correlate as well with
effects as PbB values.
One of the most difficult problems in the quantification of human
exposure is inherent in the analytical techniques, and laboratory and
sample contamination. This has been noted numerous times in the litera-
ture. Keppler (1970) reported the results of interlaboratory analyses
tor lead in blood and found that results from 60% of the laboratories
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were unacceptable. More recently, Settle and Patterson (1980) have
discussed this problem in the analysis of albacore. They reported a
1000-fold error in the lead concentration reported by the National
Marine Fisheries Service (NMFS) when it dissected, handled, and analyzed
the specimen. Settle and Patterson (1980) attributed a 20-fold error
to improper sample preparation and a 50-fold error to improper analyses.
These authors suggest that such errors are widespread and have led to
an underestimation of exposure as a result of anthropogenic sources.
This section will attempt to identify the routes of exposure to
lead for humans. In addition, attempts will be made, based on the
literature, to identify the major routes of exposure in varying situa-
tions. It is particularly difficult to assess the routes of exposure
for children because certain behavior patterns are not well studied or
quantified; e.g.,the composition of the diet and behavioral aspects
(i.e., pica, contact with dust).
The known exposure routes for humans are summarized in Figure 5-1.
Note that the routes are numerous and complex. Although food is
generally considered the largest source of lead in exposure to adults,
none of these routes can be considered minor, because both drinking
water and air can result in more significant exposures in some situations.
Similarly, the consumption of paint chips is considered the largest expo-
sure route of lead for children; however, other routes, including contact
with dust and dirt, may be significant. In general, exposure through
percutaneous absorption, as well as exposure to alkyl lead compounds,
are thought to be important only in occupational settings (WHO 1977).
Thus, these two exposure routes will not be discussed here.
The following sections will consider exposure of humans to lead
through food, drinking water, air, the ingestion of nonfood substances,
and miscellaneous sources. Because these subjects have been reviewed
extensively (WHO 1977, Mahaffey 1978, U.S. EPA 1977, Tsuchiya 1979,
NRC 1980), these reviews have been used here to avoid duplication of
effort and have been supplemented with pertinent work from the recent
literature.
5.2.2 Populations Exposed Through Food
5.2.2.1 Pathways of Exposure
Intake of lead in food is thought to be the primary pathway for
adults not employed in lead-related industries and for children without
pica (Mahaffey 1978). Sources of lead in food are numerous and the
pathways from the original source to the diet are sometimes complex
(see Figure 5-1). In general, lead can either be taken up through
surface deposition on the plant or through the roots (see Chapter 4.0).
Foods of animal origin (meats, unprocessed milk, eggs) are generally
lower in lead (Mahaffey 1978). Sources of lead in the diet include
contamination resulting from lead-soldered cans, past use of lead
arsenate pesticides, deposition on soil or plants from such sources as
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Source: Moore (1979).
FIGURE 5-1 POPULATION EXPOSURE ROUTES FOR LEAD
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automobile and smelter emissions, contamination of moonshine whiskey,
leaching from improperly glazed earthenware, and uptake from lead in
cooking water (Mahaffey 1978, Moore 1979).
Although each of these routes has been important in certain
instances, and, in some cases, fatal, the contamination of food through
the use of lead solder in cans represents the most widespread source of
lead in the diet. In 1975, the Federal Drug Administration (FDA)
estimated that canned foods comprise 11-12% of a person's diet after
1 year of age; however, the lead resulting from these foods comprises
30% of the average dietary intake of lead. More recently, the FDA has
said that lead-soldered cans are used to package 10-15% of all food,
and they contribute about 14% to the total lead ingested (Anonymous
1979a). Settle and Patterson (1980) have estimated that canned foods
comprise about 20% of the diet, and that 50% of the lead in the American
diet originates from lead-soldered cans. According to Settle and
Patterson (1980), the lower percentage estimated by the FDA may be a
reflection of their overestimation of uncontaminated food sources.
Mitchell and Aldous (1974) examined the contents of 256 metal cans
and reported that 62% of them contained lead at concentrations 100 ug/1,
37% >200 ug/1, and 12% >400 ug/1. In contrast, only 1% of products in
glass or aluminum containers had lead concentrations >200 ug/1. The
same authors conducted a survey of milk and reported that bulk milk
contained a mean lead concentration of 40 vg/1. Other authors found
that a normal level for milk was 2-10 ug/1 lead (Harding 1978). However,
canned evaporated milk contained a mean lead concentration oi: 202 ug/1-
The difference can be attributed to contamination in processing and from
the lead solder. Similar results have been reported in baby food, with
a mean concentration of 202 ug/1 for canned-food items, and a mean
concentration of 35 ug/1 for bottled foods (Mitchell and Aldous 1974).
Settle and Patterson (1980) found that tuna in lead-soldered cans con-
tained 1400 ug/kg lead (wet weight); however, tuna packed in a die-
punched unsoldered can contained 7 ug/kg lead. These results did not
represent a survey of levels in tuna.
It is apparent that lead-soldered cans represent an important
source of lead in the diet; however, the contribution from this source
is highly variable. To complicate matters further, the FDA reported
that higher concentrations of lead were found in foods stored in opened
cans than in unopened cans (Anonymous 1979b). Thus, persons who store
foods in opened cans (lead-soldered) may be exposed to higher levels of
lead in foods than some studies have indicated.
Automobile exhaust, as a source of lead deposition on plants and
soil, is important in some areas where traffic volume is higher. For
example, Rabinowitz (1974) estimated that in Southern California, 60-70%
of lead in oat tops and 80% of lead in lettuce leaves were attributed to
automobile exhaust. The absorption of lead'in air depends highly on the
type of crop. In addition, elevated concentrations in plants are observed
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within 100-200 meters of the highway (see Chapter 4.0). Still, it is
not possible to identify what portion of the diet contains lead as a
result of automobile emissions, even though it is evident, in some
cases, that this portion could be high.
Food contamination resulting from other sources of lead, such as
smelters, can also be important. Elevated levels in plants appear to
be spread over a wider area from these sources (see Chapter 4.0). As
an example of levels resulting from a smelter area, Roberts et al.
(1974) found mean levels of 2.9 mg lead/kg (fresh weight) in~Tett"uce
leaves from a smelter area, as compared with mean levels from the urban
control area of 0.9 mg/kg lead. On the other hand, no difference was
observed in lead levels in tomatoes from the two areas. Leafy vegetables,
however, retain larger amounts from air deposition (Rabinowitz 1974).
Again, it is difficult to identify what portion of the diet of persons
living near smelters can be attributed to lead emissions.
Past uses of lead arsenate as a pesticide have resulted in accumula-
tion of lead in the soil (see Chapter 4-0). This source of lead can
result in food contamination in crops cultivated in areas where lead
arsenate was used. Elfving and co-workers (1978) have reported elevated
concentrations of lead (over controls) in carrots and millet grown on old
orchard soils (7.1 and 6.8 mg/kg lead dry weight). However, the soil in
these cases contained 218 mg/kg lead. Considerably higher concentrations
of lead have been reported in other orchard sites.
The number of people exposed to high levels of lead as a result of
beverages contaminated because of improperly glazed earthenware and
distilling and uptake from cooking water is probably small compared
with the pathways described above. However, they can be extremely
serious, and, in certain situations, they are sometimes fatal. The
storage of acidic foods in earthenware has resulted in clinical lead
poisoning (Mahaffey 1978); however, no estimates of intake have been
made from such incidents. On the other hand, lead contamination of
distilled alcoholic beverages are somewhat better studied. Ball and
Sorenson (1969) estimated that 70 million gallons of "moonshine" are
produced annually. Sandstead and co-workers (1970) found that 30% of
the moonshine samples tested contained lead concentrations >1 mg/1.
Consumption of 1 I/day would result in an intake of 1 mg/day of lead.
Commercially available wines also contain lead averaging -0.2 mg/1
(Mahaffey 1978, U.S. EPA 1977). Exposure to lead from this source
could result in an intake of 0.2-1 mg/day, depending on the amount of
wine consumed (1-5 liters).
The uptake of lead by food cooked in contaminated water has not
been quantified; however, Moore (1979) reported that most foods show a
positive uptake of lead from contaminated cooking water. Because most
waters contain concentrations <0.05 mg/1, this exposure pathway is not
expected to be significant.
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5.2.2.2 Total Dietary Intake -- Adults
Over the past 30-40 years, various authors have estimated dietary
intake of lead in adults. WHO (1977) and Mahaffey (1978) provide a
detailed review of these studies; thus, they will not be discussed in
detail here. In addition, because of analytical problems, some of the
older estimates may be suspect.
Tepper (1971) estimated an average intake of 137 ue/dav.
Kolbye jet al. (1974) estimated average intakes of 57-233 yg/day,
depending on how the trace and undetected values were dealt with.
Gross (1979) reporting the results of the Kehoe lead balance experi-
ments, found an overall average dietary intake of 180 yg/day (159 yg/day,
using median data). These estimates of dietary intake represent the mean
or typical intake. Thus, it is apparent that the "average" adult con-
sumes 100-200 ug lead/day in food. However, Gross (1979) reported a
maximum intake (mean for an individual) of 334 yg/day.
Intake does vary greatly betx>reen individual and on a daily basis.
Up to 50% of this intake may be a result of lead solder in cans. The
remaining intake cannot be allocated to particular sources; however, it
probably results from contamination during processing and the other
sources described above.
In addition, persons living near areas of high lead emissions may
ingest even higher doses of lead. Kerin (1972) found that the persons
living near a lead smelter ingested 640-2640 yg/day in the diet, probably
as a result of the contamination of local crops.
5.2.2.3 Total Dietary Intake — Infants and Children
Kolbye and co-workers (1974) estimated dietary intake of 6-month-
old children eating adult table food and infant foods. These authors
found that the average intake ranged from 100-140 yg/day. Stewart and
Skeberdis (1975) found that infants from 1-12 months consumed 93 ± 36
yg/day. Boppel (1975) estimated that a 6-month-old infant (7.2 kg) fed
commercial baby food would have a lead intake of 45 yg/day. Breast-fed
infants are probably exposed to somewhat lower levels of lead (Moore
1979, Walker 1980), in general, because breast milk has been shown to
contain 6-59 yg/1 lead. Canned milk or formula would contain higher
concentrations of lead, perhaps in the range of 200 yg/1 as reported by
Mitchell and Aldous (1974) for evaporated milk. Walker (1980) found a
range of 50-500 yg/1 in canned infant formula. Formula diluted with
water would generally contain less than 50 \ig/l. However, concentrations
may be much higher in formula diluted with contaminated water, similar to
concentrations reported for electric kettles. The use of these products
in preparing infant formula has resulted in severe lead poisoning (Wigle
and Charlebois 1978).
Older children may be exposed to somewhat lower levels of lead in
food. Kolbye and co-workers (1974) estimated a dietary intake of
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75 yg/day for a 2-year-old child. Mahaffey (1976) studied children
aged 6-47 months. In 1975, she found a daily intake ranging from 12-
505 yg Pb/day with a mean intake of 110 ug/day, and a median of 76 pg/
day. In 1976, a similar study showed a range of 11-719 yg/day, with a
mean intake of 115 yg/day and a median of 95 yg/day. Lead intake for
the highest decile was 316 yg/day (Mahaffey 1976).
The specific sources associated with lead in the diet of children
are unknown. However, lead solder in cans is likely to be at least as
significant a source for children as it is for adults (up to 50% of
dietary intake). For an infant consuming canned formula, this source,
as well as contamination during processing, would result in 100% of
the dietary intake.
5.2.3 Populations Exposed Through Drinking Water
5.2.3.1 Pathways of Exposure
Surface and groundwaters in the United States generally contain
low concentrations of lead (see Chapter 4.0). Similarly, 25% of the
2595 tap water samples contained undetectable levels of lead. However,
41 of these samples contained concentrations >50 yg/1, perhaps serving
around 2% of the population (U.S. DREW 1970). Lead service lines,
plumbing, solder, and storage containers can result in contamination
of drinking water. In general, these lead concentrations are related
to pH and hardness of the water, the length of the household lead pipe.
the amount of lead in the pipe, and the position of the pipe. A low pH
is generally considered the most important factor that contributes to'
high concentrations of lead in drinking water.
The presence of a low pH and soft water is well known in the Boston
and Seattle areas. Greathouse et. al. (1976) reported that drinking
water from 25% of the households sampled in Boston exceeded 50 yg/1, and
Dangel (1975) reported that 24% of the water in Seattle exceeded this
level.
Cambridge and Somerville, Massachusetts also have had high levels
of lead in drinking water; 14.5 and 30% of the households surveyed
showed water lead levels of greater than 50 yg/1. It has been estimated
that about half of the buildings in these cities have some lead service
pipe. The initiation of pH adjustment in 1975, however, reduced the
lead levels in households that had exceeded the standard to less than
about 20 yg/1 in Cambridge (Karalekas et al. 1976).
Other cities with levels of lead greater than 50 yg/1 have also
been reported, including Worcester, Massachusetts (O'Brien 1976);
Bennington, Vermont (Taylor 1977), and New Bedford, Massachusetts
(Karalekas et al. 1978). Rural water supplies have also been identi-
fied as having elevated lead levels in drinking water, such as
Chesterfield County, South Carolina, where 10.3% of the 217 samples
taken exceeded 50 yg/1 (Sandhu _et al. 1977).'
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The prevalence of elevated lead levels in drinking waters in the
United States today is difficult to evaluate for several reasons. One,
the use of lead pipes is not well documented. In a survey of water
utilities reported by Donaldson (1924), 51% of the 539 cities surveyed
indicated that they used lead or lead-lined services to some extent.
It is unlikely that the situation has changed drastically since that
time. Patterson and O'Brien (1979) reported that nearly half of the
100 largest cities in the U.S. distribute corrosive water, and many have
some portion of lead pipes. Thus, it appears that there is a potential
for a large portion of the population to receive lead at levels greater
than 50 yg/1 in drinking water. However, such approaches as pH adjust-
ment and treatment with zinc orthophosphate are being used to control
corrosion (Karalekas _e_t _al. 1976).
5.2.3.2 Drinking Water Exposure — Adults
Drinking water is sometimes included in the estimates of dietary
exposure described above. Often, this is not well documented, however.
for the purposes of this report, a consumption of 2 I/day water will be
assumed for adults, in addition to the dietary consumption of lead.
Thus, most adults would ingest <20 ug/day lead in drinking water. Al-
though the population sizes are unknown, a small proportion of the popu-
lation would be exposed to 100 ug/day from this source, and an extremely
limited subpopulation would be exposed to 2 mg/day in drinking water.
5.2.3.3 Drinking Water Exposure — Infants and Children
A drinking water consumption of 1 I/day will be assumed for infants
and children, thus reducing the intakes estimated above by one-half.
Therefore, the respective subpopulations would receive <10 ygVday,
50 yg/day, and 1 mg/day in drinking water.
5.2.4 Populations Exposed Through Inhalation (Air, Dirt, and Dust)
5.2.4.1 Pathways of Exposure
The major source of lead in the atmosphere is automobile emission
(see Chapters 3.0 and 4.0). Local contamination of air around smelters,
battery manufacturers, etc. also results in human exposure. Adults are
directly exposed through inhalation of ambient air. The exposure pathway
for children is far more complicated because deposited particulates
result in contamination of dust and dirt. Intentional or inadvertent
ingestion of lead from this source is not easily quantified and will be
discussed later in this section.
Concentrations of lead reported in air have been discussed in
Chapter 4.0. The U.S. EPA (1977) also provides a discussion on this
subject. For the purposes here, various concentrations typical of
certain situations have been assumed (see Table 5-1).
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1
1
1
^B
1
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1
1
1
1
1
TABLE
S ub populat ion
Smelters, battery
etc.
Urban
Outdoors
Indoors0
TOTAL
Rural (suburban)
Outdoors
Indoors
TOTAL
Remote
alnhalation of 20
outdoors.
h
5-1. HUMAN EXPOSURE TO LEAD THROUGH INHALATION
Cone Inhalation Adults3 Inhalation Childb
(jig/m3) (yg/day) (yg/day)
operations, 10 200 40
1-4 13-53 2.7-10.8
0.3-1.4 2-9.4 0.4-1.8
15-62 3.1-12.6
0.1-1 1.3-13 • 0.3-3
0.03-0.3 0.2-2 .04-0.4
1.5-15 .34-3.4
<-02 0.4 0.08
m /day assumed for adults spending 1/3 time indoors, 2/3
T
Inhalation of 4 m /day for 1-year old child spending 1/3 time indoors, 2/3
outdoors.
Concentrations assumed to be 1/3 outdoors.
t
I Source: See Section 4.2.2 for concentrations of lead in air.
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5.2.4.2 Inhalation Exposure — Adults
Inhalation estimates of lead for adults have also been described I
in Table 5-1. A respiratory flow of 20 m3/day was assumed. Potential •
exposure appears to be highest in urban areas*and near lead-related
industries. •
5-2.4.3 Inhalation Exposure — Infants and Children
Inhalation for a one-year-old child was assumed in Table 5-1. The |
patterns of exposure are the same as those seen in adults. Older
children would experience increasingly high total exposure to lead. m
5.2.5 Populations Exposed Through Other Routes
5.2.5.1 Cigarettes •
Lead has been reported in cigarettes at concentrations up to
39 mg/kg (Cogbill and Hobbs 1957). This has been primarily attributed •
to past uses of lead arsenate (Mahaffey 1978, WHO 1977). WHO (1977) "
estimated, assuming a 27, transfer rate from mainstream smoke, that a
person smoking 20 cigarettes/day would inhale 1-5 yg/day. •
5.2.5.2 Dirt and Dust
Lead reaches dirt and dust through various pathways (see Figure 5-1). I
Of particular importance are automobile and smelter emissions and losses
from painted surfaces that result in soil contamination. Monitoring —
data (see Chapter 4.0) have shown that levels approaching 8,000 mg/kg I
in soil can result in the vicinity of such sources. Household dust and ™
street dust also exhibit elevated concentrations. Old orchard sites and
manufacturing sites may also have high levels of lead. M
These levels are probably not of great significance for adults;
however, children are susceptible to this exposure route through inges-
tion of dirt and dust, and mouthing of contaminated hands and other
objects. Lepow_et al. (1974) examined ten children with chronically
high PbB levels. These authors determined that nine of the ten children
studied exhibited excessive mouthing. Three of the children had their
hands or nonfood items in their mouths during 50% of the observation
time. The mean lead in the samples from the childrens1 hands was
2400 yg/g. This study estimated that if a small child playing in dirt
with a lead concentration of only 1200 yg/g mouthed his fingers 10 times/
day, ingesting 10 mg of dirt/mouthing, this child would ingest 120 yg/day
of lead. The same calculation using household dust (with a concentration
of 11,000 yg/g) would result in an exposure of 1100 yg/day (Lepow et al.
1974). Unfortunately, little is known about such behavior patterns~~of~
children. These estimates, however, do not appear unreasonable and may
be common in areas with contaminated soil and dust.
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5.2.5.3 Paint
The ingestion of paint chips by children is commonly thought to be
the most prevalent route of lead exposure for children in the United
States today. Paints used before World War II contained lead at levels
greater than 1% (10,000 mg/kg). In 1974, a marketplace survey found
that 70.8% of the oil-based paints and 96.1% of the water-based paints
sampled contained< 0.06% lead, which is the recommended maximum permis-
sible level in paint (Committee on Toxicology 1976). However, numerous
old buildings still exist with chipped and peeling paint that contain
higher levels of lead. Gilsinn (1972) estimates that 7 million housing
units are old enough to contain high levels of lead.
This problem is especially severe for children having pica. It
appears common in children, especially l-to-3-year-olds; estimates suggest
that one-third to one-half of the children in this age bracket have pica.
Unfortunately, little is known about the amount of paint ingested.
However, only small amounts (a 1-milligram chip) of paint containing
l%^lead are required to result in an exposure of 1 mg/day (Mahaffey
1978). Such an exposure would probably be common in children having
pica and who are exposed to lead at such levels.
5.2.5.4 Other Routes
Numerous other exposure routes for lead are generally considered
to be minor. For example, ingestion of newsprint, curtain weights,
lead paint on kitchen utensils, decorative decals, and lead stearate
used in PVC pipes can all result in exposure to lead (WHO 1977, Mahaffev
1978). These exposure routes are expected to be important only in
isolated situations and have not been included here.
5-2.6 Blood Levels Associated with Various Subpopulations
Bell and co-workers (1979) report a survey of the literature shows PbB
levels in rural or urban areas in the range of 9-24 ug/100 ml with most
values vL6 ug lead/100 ml blood. Gross (1979) reported an overall mean PbB
level in a sample of adults of 25 ug/100 ml, and individual mean levels
ranged from 18-40 ug/100 ml. WHO (1977) estimated that each 100 ug of oral
intake from dietary sources contributes about 6-18 ug of lead/100 ml of
blood. Thus, as expected, dietary intake accounts for most of the lead
in the blood of adults.
In addition, numerous studies have been conducted to determine the
importance of air concentrations in contributing to lead in blood.
These studies are reviewed in U.S. EPA (1977) and Bell et al. (1979)
and will not be discussed in detail here. In total, these studies
appear to indicate that the contribution of air lead to blood lead
ranges from 0.6-2.0 ug/100 ml in blood/ug lead/m3 in air. In general,
blood lead concentrations do not correlate well with air concentrations
because the effects are masked by intake from other sources, primarily
food. However, urban levels of blood lead have been shown to be
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significantly higher than suburban levels (Tepper and Levin 1972).
The geometric mean blood lead (age and smoking adjusted) for urban
areas was 18 yg/100 ml and 16 ug/100 ml for rural. Assuming a log-normal
distribution, <5% of the urban population would have PbB levels >30 yg/
100 ml; and <0.5% of the rural population (U.S. EPA 1977).
A relationship between blood lead and distance from highways has
also been observed. Daines and co-workers (1972) found that mean PbB
levels for black women living 3.7, 38.1, and 121.9 meters from a highway
were 23.1, 17.6, and 17.4 yg/100 ml, respectively.
Levels of blood lead in persons living near smelters are also
elevated. Landrigan et al. (1975) found that 16% of the individuals
over 19 living near the smelter in El Paso, Texas had PbB levels
>40 yg/100 ml.
In addition, relationships between blood lead and levels in drinking
water have been observed. Moore and co-workers (1977) found that the
mean PbB level rose as the cube root of the "first draw" of water. Thus,
they estimated that PbB levels at water concentrations of 50 and 100 yg/1
would be about 20 yg/100 ml and 22 yg/100 ml, respectively. Although
this may represent a significant difference, the example indicates that
drinking water does not contribute greatly to lead exposure in adults,
except at very high concentrations.
In general, elevated PbB levels (>15 yg/100 ml) have been related
to such factors as residency in urban areas, near highways, and near
smelters. Blood levels of lead >40 yg/100 ml in adults are found in
these areas.
Blood levels of lead in children are consistently higher than those
of adults in the same environment. Lead screening programs detect about
40,000 children annually with PbB levels >30 yg/100 ml. However, this
figure represents only a proportion of those children in the United
States who actually exceed this level. McFeatters (1976) reports that
the U.S. Department of Housing and Urban Development estimates that at
least 600,000 U.S. children have high levels of lead in their blood.
The preceding discussion indicates that the largest route of exposure
for children with pica is the ingestion of paint, dirt, and dust. The
source of this contamination is primarily paint in rural areas, auto-
mobile emissions in urban areas, and smelter or other industrial
emissions near sources. Numerous studies have been conducted to
determine the relative importance of these various routes and sources.
Again, these have been described extensively in U.S. EPA (1977) and
Bell e£ _al. (1979) and will only be discussed briefly here.
The distance of residence from a highway has been correlated with
PbB levels of children. Caprio and co-workers (1974) found that >57%
of the children living within 100 feet of roadways had PbB levels
>40 yg/100 ml. More than 27% of those living 100-200 feet from the
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highway and 31% of those living greater than 200 feet away had similar
levels. Although this study indicated a localized effect on PbB levels,
the pathway of exposure could have been inhalation or ingestion of dirt
and dust.
Billick and co-workers (undated-a) examined 170,000 records from
1976 of children's PbB levels in New York. These authors found that
blacks had higher PbB levels than whites or Hispanics. In addition, a
peak in PbB levels was observed during the summer each year. The highest
PbB levels were found in the 2-to-4-year-old age bracket. In addition, a
general downward trend was observed in PbB levels during these years.
This was attributed to the lead screening program, decrease in paint
exposure, and changes in environmental lead exposure. The air lead
concentrations, ethnic group, and age were highly significant factors
in determining PbB levels and explained 63-65% of the variation in PbB
levels.
In a follow-up study, Billick and co-workers (undated-b) evaluated
lead in gasoline as an indicator of exposure. They found that gasoline
lead (as measured by sales) is a highly significant variable. They
developed a model that explained 75% of the variation in PbB level by
age, race, season, and leaded gasoline sales. Using the model, these
authors estimated the geometric mean concentration for children in the
absence of gasoline lead to be 10.1 pg/100 ml for the first quarter.
In comparison, the yearly geometric mean for black, Hispanic, and white
children of the same age was 21.2, 19.2, and 19.3 ug/100 ml, respectively.
These results suggest a reduction of about 50% in childrens' PbB levels
in urban areas with the phasing out of lead in gasoline. The ambient air
contributed little to the variation in blood, after gasoline lead had
been considered. These authors suggest that inhalation was only secon-
dary to ingestion of dirt and dust.
Angle and Mclntire (1979) investigated the correlation of childhood
PbB level with lead in air, soil, and house dust. A multivariate analysis
showed that PbB levels for preschool children was positively correlated
with house dust and soil (11% of the variance) and PbB levels in children
6-18 was significantly correlated with air, soil, and house dust (21% of
the variance). However, 38% of the variation was a result of the differ-
ence between samples from an individual.
The U.S. EPA (1977) concluded that observable increases in PbB
levels occur at soil or dust lead exposures of 500-1000 mg/kg. In a
summary of soil lead/blood lead relationships on children, these authors
found a mean increase of 3-6% in lead blood for a two-fold increase in
soil lead levels.
Lead paint is a well known source of elevated blood levels in
children (U.S. EPA 1977, WHO 1977, Bell et_ al. 1979). In general,
however, the contribution of paint to levels in blood is difficult to
distinguish from the contribution of lead in soil and dust, especially
in urban areas. Cohen and co-workers (1973) found that the mean PbB
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level for 230 children (1-5 years old) in two rural counties was
22.8 ± 11.0 ug/100 ml. More than one-half of the children lived in
houses more than twenty-five years old, one-quarter of which had flaking
paint or plaster. The presence of lead in paint or plaster is not the
only condition that must be met to increase levels of lead in the blood;
the paint must also be peeling or chipping. In addition, for exposure
to occur, it must be ingested. As a result, it is difficult to correlate
lead in paint with PbB levels in children (U.S. EPA 1977).
Children with high PbB levels are also concentrated around indus-
trial sources of lead, especially smelters. Most recently, Walter and
co-workers (1980) studied PbB levels in the areas surrounding a primary
lead smelter in the Idaho Silver Valley. These authors found that 98.9%
of the children surveyed in 1974 (ages 1-9) that resided closest to the
smelter had PbB levels >40 ug/100 ml and 59.7% had levels >60 ug/100 ml.
A multiple regression analysis for each year of age showed that air lead
was the most significant variable influencing PbB level. The next most
important variable was levels of lead in household dust, primarily in
children younger than four. Soil lead was also a significant factor in
determining blood lead. Pica was significant at age 2 years, and 25%
increase in blood lead was predicted in a child with pica. In addition,
sex, and occupation of the parent were significant variables,. These
authors also noted that inhalation is probably not the major pathway of
absorption. Lead was apparently deposited and ingested.
A follow-up survey conducted in 1975 showed that PbB levels were
somewhat reduced, probably because of emigration, treatment of children
with high PbB levels, increased cleanliness, replacement of highly
contaminated topsoil, and reduction of lead emissions (Walter jet al.
1980). Today, almost all children have PbB levels <60 ug/100 ml, and
most have levels <40 ug/100 ml (Anonymous 1979a).
Similar results, although less severe, have been reported from the
lead smelter in El Paso, Texas. About 70% of the children 1-4 years old
living near this smelter had PbB levels >40 ug/100 ml, and 14% had PbB
levels >60 ug/100 ml (Landrigan et al. 1975).
Baker and co-workers (1977) examined lead absorption in children in
nineteen U.S. towns with primary nonferrous smelters and compared them
with children of the same age in towns without smelters. This included
all primary lead, zinc, and copper smelters, with the exception of the
smelters in El Paso, Texas, Kellogg, Idaho, Tacoma, Washington, and East
Helena, Montana, because these towns had already been studied. They
found that PbB levels were significantly elevated in children living
around two zinc smelters, but not near the two lead smelters. However,
hair-lead levels were elevated in these areas.
Elevated lead levels have also been reported in the vicinity of
secondary smelters and battery plants (U.S. EPA 1977). PbB levels
>30 ug/100 ml appear to be common in these areas.
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In summary, elevated lead levels (a term difficult to define, but
generally meaning >30 yg/1) have been reported in numerous situations
for children. Exposure to lead-containing paint, dirt, and dust are
probably the major sources of exposure. Contaminated dirt and dust can
result from paint, automobile emissions, and industrial emissions from
such sources as primary and secondary smelters and battery plants.
5.2.7 Summary — Exposure Scenarios
5.2.7.1 Introduction
This section will attempt to isolate certain subpopulations and
determine their total exposure to lead. In addition, an attempt will
be made to identify important routes and sources of exposure. Although
these situations are somewhat hypothetical, they are based on the data
available in this section and the preceding ones in order to represent
typical examples of exposure.
This section concentrates on total intake; however, for comparison
of routes, the absorbed dose must be considered. As discussed in the
previous section, the absorption of lead depends on a number of factors,
such as particle size, physiochemical form of lead, route, and extent
of exposure, as well as host factors, such as age and nutritional status.
For the estimates presented here, absorption of lead from the gastro-
intestinal tract of adults will be assumed at 10%. Absorption of
ingested lead by children is assumed to be 50%. Deposition of inhaled
lead is assumed to be 30% and 100% of deposited lead is assumed to be
absorbed. Little is known about absorption of inhaled lead by children;
however, it is assumed to be the same as adults, although it may be
greater.
5.2.7.2 Exposure Estimates
Exposure estimates for children and adults in different situations
are summarized in Table 5-2. Figures 5-2 and 5-3 show the estimated
exposure for adults and children living in rural, urban, and industrial
(smelters, etc.) environments. The relative importance of the various
routes are shown using the estimates derived earlier in this section.
For adults, food is the greatest source of exposure in all the exposure
scenarios shown in Figures 5-2 and 5-3. Intake of lead in food was
considered the same (200 yg/day) in urban and rural areas; however, near
smelters, it was assumed to be 1000 yg/day because of contamination of
local crops. Drinking water intakes for all the scenarios shown in
Figures 5-2 and 5-3 were assumed to be <20 yg/day, because most drinking
waters contain <10 yg/1. However, concentrations of 50 yg/1 in rural
areas would increase the contribution of lead from this source from 9 to
31%. This effect would not be as dramatic in urban and industrial areas.
Highly contaminated drinking water (1 mg/1) would overshadow all other
sources of exposure (see Table 5-2).
5-33
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TABLE 5-2. EXPOSURE ESTIMATES OK LEAD FOR ADULTS AND CHILDREN LIVING IN
RURAL, URBAN, AND INDUSTRIAL ENVIRONMENTS
Population
Adults
Location
Rural
Route
Oi
to
Urban
Food
Drinking Water
Inhalation
Food
Smelting Areas
Drinking Water
Inhalation
Food
Source
Total Diet
Moonshine
Wine
Most Supplies
Contaminated
Highly Contaminated
Suburban
Remote
Cigarettes
Total Diet
Moonshine
Wine
Most Supplies
Contaminated
Highly Contaminated
Urban Air
Cigarettes
Total Diet
Moonshine
Wine
Assumption
1 mg/1, 1 I/day
0.2 rag/1, I/day
0.2 mg/k, 5 I/day
<10 Mg/1, 2 I/day
>50 Mg/1, 2 I/day
> 1000 Mg/1, 2 I/day
See Table 5-1
See Table 5-1
-
1 mg/1, 1 I/day
0.2 mg/1, 1 I/day
0.2 mg/1 5 I/day
<10 Mg/1, 2 I/day
>50 |jg/l, 2 I/day
>1000 Mg/1, 2 I/day
Intake
(Mg/day)
100-200
1000
200
1000
<20
>100
>2000
1.5-15
0.4
-
100-200
1000
200
1000
<20
>100
>2000
Ahiiorheil Doseu
(Mg/day)
10-20
100
20
100
<2
>10
>200
0.5-5
0.1
1-5
10-20
100
20
100
<2
>10
>200
See Table 5-1
1 mg/1, 1 I/day
0.2 mg/], 1 I/day
0.2 mg/1, 5 I/day
15-62
100-2640
1000
200
1000
5-21
1-5
10-264
100
20
100
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TABLE 5-2. EXPOSURE ESTIMATES OP LEAD FOR ADULTS AND CHILDREN LIVING IN
R1IKAI., UKHAN, AND TNIHISTRIAI. KNVfKONMKNTS (Continued)
Population
Location
Route
Drinking Water
Inhalation
Source
Most Supplies
Contaminated
Highly Contaminated
Ambient Air
Cigarettes
Assumption
<1() MK/I, 2 I/day
>50 ug/1, 2 I/day
>1000 ug/1, 2 I/day
10 ng/m3, 20 m3/day
Intake
dig/day)
*20
> 100
>2000
200
Absorbed Itose
(pg/day)
<2
>200
60
1-5
Children
Rural
Pood
Total Diet
100
Cri
I
w
ui
Drinking Water
Inhalation
Most Supplies
Contaminated
Highly Contaminated
Ambient Air
<10 iig/1, 1 I/day
<50 „(./!, 1 I/day
>1000 HB/I, 1 I/day
See Table 5-1
<50
> 1000
0.34-3.4
bOO
0.1-1
Pica
lead faint
Paint or Otherwise
Contaminated Dirt
12 lead, 1 rag chip 1000
1000 ug/g lead in dirt, 100
10 mg/mouthing, 10 moutilings/
day
500
50
Urban
Food
Total Diet
100
50
Drinking Water
Most Supplies
Contaminated
Highly Contaminated
<10 ug/1. 1 I/day
<50 ug/1, 1 I/day
>1000 ug/1, 1 I/day
<50
> 1000
<5
<25
>500
Inhalation
Ambient Air
T.ihlo 5-1
3.1-12.6
Pica
Lead Paint
Dirt
Dust
IZ lead, 1 rag chip 1000
1000 ug/g lead in dust 100
10 mg/mouthing, 10 mouth ings/
day
10,000 |ig/g lead in dust 1000
10 HI;; .lust/mouthing, 10
mouth ings/day
500
50
500
-------
TABLE 5-2. EXPOSURE ESTIMATES OF LEAD KOR ADULTS AND UULDRBN LIVING IN
RURAL, URBAN, AND INDUSTRIAL ENVIRONMENTS (Continued)
Population
Location
Smelting Areas
Route
Food
Drinking Water
Source
Total Diet
Most Supplies
Contaminated
Highly Contaminated
Assumption
Assumed to be half of
adult
<10 ug/1, 1 I/day
<50 Mg/1. 1 I/day
>1000 Mg/l, 1 I/day
Intake
(ng/day)
500
<50
>1000
Absorbed Dose
(lig/day)
250
<5
<.25
>500
Inhalation
Anihlent Air
Table 5-1
12
Pica
U>
Lead Paint
Dirt
Dust
17. lead, 1 rap, chip
1000 ug/g lead In dirt,
10 ing/mouthing, 10 mouthlngs/
day 100
10.000 |ig/g lead in dnut 1000
10 nig dust/mouthing, 10
mouth ings/day
500
50
500
A 10Z absorption of Ingested lead Is assumed for adults and 50% for children. Deposition of inhaled lead Is assumed
to be 30% and 100% of deposited lead Is assumed to be absorbed.
Source: See text.
-------
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Air - 1%
Rural Areas —
20 ug/day
Drinking
Drinking Water
Water - 1%
(lead solder in
cans - 25%)
Urban Areas —40 jug/day
Food
(62%)
(lead solder in
cans - 31%)
Smelters, Lead Works, etc. — 160 Mg/day
Note: Concentrations < 10 jug/2 in drinking water were assumed for these estimates, and no con-
sumption of wine or moonshine containing lead. In addition, these situations did not include
exposure from smoking.
Source: Arthur D. Little, Inc., estimates.
FIGURE 5-2 EXPOSURE SCENARIOS - ADULTS
(ABSORBED DOSE)
5-37
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Drinking Water - 1%
Food (4%)
Drinking Water and
• Air- 1%
Paint and
Paint
Contaminated
Dirt
(90%)
Rural -560M9/day
Paint,
Dirt,
and
Dust
(94%)
Drinking Water
and Air - 1%
Smelters, Lead Works, etc. - 1300M9/day
Source: Arthur D. Little, Inc., estimates.
FIGURE 5-3 EXPOSURE SCENARIOS - CHILDREN WITH PICA (ABSORBED DOSE)
5-38
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If moonshine is consumed (1 liter containing 1 mg/l/day), this
source of exposure would be far greater than any other source. Wines
would have to be consumed in large amounts (5 I/day containing 200 ug/1
lead) in order to be the dominant exposure route in lead industrial
areas. However, consumption of 1 I/day would represent about 50% of
the total absorbed dose in rural areas, and 30% in urban areas. The
increase in total exposure from rural to urban areas is a result of
the increased exposure through inhalation; primarily due to lead
emissions from automobiles. Even in urban areas, however, food is at
least as significant a source if not more significant than air. The
increased exposure in the vicinity of smelters and perhaps other lead
industries is related to increased inhalation and perhaps increased
levels of lead in foods.
These results suggest that elimination of lead solder in cans would
reduce exposure by, at most, -6-50% in adults, depending on the subpopu-
lation exposed. In addition, the elimination of lead in gasoline would
reduce exposure in urban areas by about 35% (assuming no reduction in
solder in cans). If lead were eliminated from cans as well as from
gasoline, exposure could be reduced by about 60%. However, persons
consuming large amounts of lead in drinking xcater, moonshine, or wine
would not experience such reduction in exposure. These estimates are
only an approximation and are intended to demonstrate the relative
nature of exposure of lead to adults.
Similar exposure scenarios for children with pica are illustrated
in Figure 5-3. As expected, consumption of paint, dirt, and dust
containing lead represents the largest exposure route for these children.
Exposure to children without pica would be much lower, for example, 560 as
compared to-50 ug/day in rural areas. la urban and industrial areas,
children without pica may be exposed to somewhat higher levels than
would be expected because dirt and dust may be contaminated, and mouthing
of objects and hands can result in exposure.
In the scenarios shown in Figure 5-3, concentrations of lead in
drinking water were assumed <10 ug/1. However, higher levels in drinking
water would probably not contribute greatly to exposure for children with
pica. It would be a significant source for infants and children without
pica.
The increase in exposure from rural, urban, and industrial areas is
primarily a result of the increase in lead levels of soil and dust.
Gross estimates were made in order to evaluate the importance of this
source in total exposure to children. However, even if these estimates
were reduced by an order of magnitude, consumption of paint, dirt, and
dust would still constitute the major source of exposure for children.
5-39
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REFERENCES
Alexander, F.W.; Delves, H.T.; Clayton, B.E. The uptake and excretion
by children of lead and other contaminants. In: Proceedings of the
international symposium; Environmental health aspects of lead, 1972,
May 2-6, Amsterdam. Luxembourg, Commission of the European Communities-
1973: 319-330. (As cited in WHO 1977)
Ahlberg, J.; Ramel, C.; Wachtmeister, C.A. Organolead compounds shown
to be genetically active. Ambio 1:29; 1972. (As cited in Grand-jean
and Nielsen 1979)
Angle, C.; Mclntire, M. Environmental lead and children: the Omaha
study. J. Toxicol. Environ. Health 5:855-870; 1979.
Anonymous. Lead in canned food to be reduced. Chemical and Engineerins
News 57 (37):20; 1979a.
Anonymous. FDA-er reports lead concentrations are higher from stored
opened cans. Food Chemical News; November 19, 1979b: 23.
Amvig, E. ; Grandjean, P.; Beckmann, J. Neurotoxic effects of heavy
lead exposure determined with psychological tests. Toxicol. Lett. 5:393-
404; 1980.
Baker, E.L., Jr.; Hayes, C.G.; Landrigan, P.J.; Handke, J.L.; Leger, R.T.;
Houseworth, W.J.; Harrington, J.M. A nationwide survey of heavy metal
absorption in children living near primary copper, lead and zinc smelters.
Am. J. Epidemiol. 106:261-273; 1977.
Ball, G.V.; Sorenson, L.B. Pathogenesis of hyperuricemia in saturine
gout. New Engl. J. Med. 280:1199-1202; 1969. (As cited by Mahaffey
1978) ^
Barry, P.S.I. A comparison of concentration of lead in human tissues.
Brit. J. Ind. Med. 32:119-139; 1975. (As cited by WHO 1977)
Barry, P.S.I. Distribution and storage of lead in human tissues. The
biogeochemistry of lead in the environment. Part B. Biological effects.
Nriagu, J.D. (ed.) New York: Elsevier/North-Holland Biomedical Press;
1978: 97-150.
Barton, J.C.; Conrad, M.E. Effects of ethanol on the absorption and
retention of lead. Proc. Soc. Exp. Biol. Med. 159(2):213-218; 1978.
Bauchinger, M.; Schmid, E. Mutat. Res. 14:95-100; 1972. (As cited by
Kazantzis and Lilly 1979)
5-40
-------
I
I
I
I
I
I
I
I
I
I
I
Boyland, E.; Dukes, C.E.; Grover, P.L.; Mitchley, B.C.V. The induction
of renal tumors by feeding lead acetate to rats. Brit. J. Cancer 16:283-
• 1962. ' (As cited by IARC 1972)
I
I
I
I
I
I
Bauchinger, M.; Schmid, E.; Schmidt, D. Chromosomenanalyse bei
verkehrspohzisten mit erhohter bledast. Mutat. Res. 16:407-412' 1972
(As cited by WHO 1977).
Bauchinger, M.; Schmid, E.; Einbrodt, H.J.; Dresp, J. Chromosome aberra-
tions in lymphocytes after occupational exposure to lead and cadmium.
Mutat. Res. 40:57-62; 1976. (As cited by WHO 1977)
Beek, B.; Obe, G. Experentia 30:1006-1007; 1974. (As cited by Kazantzis
and Lilly 1979)
Bell, M.W.; Ewing, R.A.; Lutz, G.A.; Holoman, V.L.; Paris, B.; Krause, H.H.;
Hammond, P.B. Reviews of the environmental effects of pollutants: VII.
Lead. Report No. EPA-600/1-78-029. Columbus, OH: U.S. Environmental
Protection Agency; 1979. 476 p. Available from: NTIS, Springfield, VA-
PB80-12107 2.
Billick, I.E.; Curran, A.S.; Shier, D.R. Pediatric blood lead levels in
New York. (Submitted for publication) Washington, DC: Environmental
Research Group, Department of Housing and Urban Development; undated-a.
Billick, I.E.; Curran, A.S.; Shier, D.R. Relation of pediatric blood
lead levels to lead in gasoline. (Submitted for publication) Washington,
DC: Environmental Research Group, Department of Housing and Urban
Development; undated-b.
Bolanowska, W. Distribution and excretion of triethyllead in rats.
Brit. J. Ind. Med. 25:203-208; 1968. (As cited by WHO 1977)
Boppel, B. Bleigehalte von lebensmitteln in bleiaufnahme durch die
tagliche Nahrung. Z. Lebensm.-Unters. Forsch. 158:287-290; 1975. (As
cited by Mahaffey 1978)
Bushnell, P.J.; Bowman, R.E. Persistence of impaired reversal learning
in young monkeys exposed to low level of dietary lead. J. Tox. Environ.
Health 5(6):1015-1023; 1979.
Bushnell, P.J.; Shelton, S.E.; Bowman, R.E. Elevation of blood lead
concentration by confinement in the rhesus monkey. Bull. Environ.
Contam. Toxicol. 22:819-826; 1979.
Butt, E.M.; Peason, H.E.; Simonsen, D.G. Proc. Soc. Exp. Biol. Med.
79:247-249; 1952. (As cited by Rosen and Sorell 1978)
Butt, E.M.; Nusbaum, R.E.; Gilmour, T.C.; Didio, S.L.; Sister Mariano.
Trace metal levels in human serum and blood. Arch. Environ. Health
8:52-57; 1964. (As cited by WHO 1977)
5-41
-------
Caprio, R.J.; Margulis, H.L.; Joselow, M.M. Lead absorption in children
and its relationship to urban traffic densities. Arch. Environ. Health
28:195-197; 1974. (As cited by U.S. EPA 1977)
Cavalleri, A.; Minoia, C.; Pozzoli, L.; Polatti, F.; Bolis, P.F. Lead
in red blood cells and in .plasma of pregnant women and their offspring.
Environ. Res. 17(3):403-408; 1978.
Center for Disease Control. Surveillance of childhood and lead poisoning.
U.S. Morbid. Mortal. Week. Rep. 26:48; 1977. (As cited by U.S. EPA 1979)
Chisolm, J.J., Jr. Heme metabolites in blood and urine in relation to
lead toxicity and their determination. Adv. Clin. Chem. 20:225-265-
1978.
Chisolm, J.J., Jr.; Barltrop, D. Recognition and management of children
with increased lead absorption. Arch. Dis. Child 54(4):249-262; 1979.
Clarkson, T.W.; Kench, J.E. Urinary excretion of amino acids by men
absorbing heavy metals. Biochem. J. 62:361-372; 1956. (As cited fav
WHO 1977)
Cogbill, E.G.; Hobbs, M.E. Transfer of metallic constituents of
cigarettes to mainstream smoke. Tob. Sci. 144:24-29; 1957. (As cited
by Mahaffey 1978).
Cohen, M.M. Biochemical aspects of lead neurotoxicity. Handb. Clin.
Neurol. 36:65-72; 1979.
Cohen, G.J.; Bowers, G.N.; Lepow, M. Epidemiology of lead poisoning.
J. Am. Med. Assoc. 266:1430-1433; 1973. (As cited by WHO 1977)
Coleman, I.P.L.; Hilburn, M.E.; Blair, J.A. The intestinal absorption
of lead. Biochem. Soc. Trans. 6(5):915-917; 1978.
Committee on Toxicology, Assembly of Life Sciences, National Research
Council (NRC). Recommendations for the prevention of lead poisoning
in children. Washington, DC: National Academy of Science; 1976. (As
cited by Mahaffey 1978).
Cooper, W.C. Mortality in workers in lead production facilities and
lead battery plants during the period 1971-1975. A report to Inter-
national Lead Zinc Research Organization, Inc.; 1978. (As cited by
U.S. EPA 1980)
Cooper, W.C. Occupational lead exposure: what are the risks? Science
208:129; 1980.
Cooper, W.C.; Gaffey, W.R. Mortality of lead workers. Occup. Med.
17:100; 1975. (As cited by U.S. EPA 1980)
5-42
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I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Cramer, K.; et al. Renal ultrastructure, renal function and parameters
of lead toxicity in workers with different periods of lead exposure.
Br. J. Ind. Med. 31:113; 1974. (As cited by U.S. EPA 1980)
Cremer, J.E. Toxicology and biochemistry of alkyllead compounds. Occup
Health Rev. 17:14-19; 1965. (As cited by WHO 1977)
Daines, R.H.; Smith, D.W.; Feliciano, A.; Trout, J.R. Air levels of lead
inside and outside of homes. Ind. Med. Surg. 41:26-28: 1972. (As cited
by U.S. EPA 1977)
Damstra, T. Toxicological properties of lead. Environ. Health Persp.
19:297-307; 1977. H
Dangel, R.A. Study of corrosive products in the Seattle water department
Tolt distribution system. Report No. EPA-670/2-75-036. Cincinnati, OH:
U.S. Environmental Protection Agency; 1975. (As cited by Mahaffey 1978)
Deknudt, G.; Leonard, A.; Ivanov, B. Chromosome aberrations observed in
male workers occupationally exposed to lead. Environ. Physiol. Biochem
3:132-138; 1973. (As cited by WHO 1977)
Deknudt, Gh.; Manuel, Y.; Gerber, G.B. Chromosomal aberrations in workers
professionally exposed to lead. J. Toxicol. Environ. Health 3(5-6):885-891;
JL*7 / / *
De la Burde, B.; Choate, M.S. Does asymptomatic lead exposure in children
have late sequelae? J. Pediatr. 81:108; 1972. (As cited by U.S. EPA 1980)
De la Burde, B.; Choate, M.S. Early asymptomatic lead exposure and
development at school age. J. Pediatr. 87:638; 1975! (As cited by
U.S. EPA 1980)
Der, R.; Fahin, Z.; Hilderbrand, D. Combined effect of lead and low
protein diet on growth, sexual development and metabolism in female rats.
Res. Commun. Chem. Pathol. Pharmacol. 9(4):723-738; 1974. (As cited bv
U.S. EPA 1977)
Dietz, D.D.; McMillan, D.E.; Grant, L.D.; Kimmel, C.A. Effects of lead
on temporally-spaced responding in rats. Drug Chem. Toxicol. 1(4):401-
419; 1978.
Dingwall-Fordyce, J.; Lane, R.E. A follow-up study of lead workers
Br. J. Ind. Mech. 30:313; 1963. (As cited by U.S. EPA 1980)
Dipaolo, J.A.; Nelson, R.L.; Casto, B.C. In vitro neoplastic transforma-
tion of Syrian hamster cells by lead acetate and its relevance to environ-
mental carcinogenesis. Br. J. Cancer 38(3):452-455; 1978.
5-43
-------
Donaldson, W. The action of water on service pipes. Journal AWWA 11:
649; 1924. (As cited by Patterson and O'Brien 1979)
Earl, F.L.; Vish, T.J. Teratogenicity of heavy metals. Toxicity of
heavy metals in the environment. Part 2. Oehme, F.W. (ed.) New York,
NY: Marcel Dekker, Inc.; 1979: 617-639.
Elfving, D.C.; Haschek, W.M.; Stehn, R.A.; Bache, C.A.; Lisk, D.Jo
Heavy metal residues in plants cultivated on and in small mammals indi-
genous to old orchard soils. Arch. Environ. Health 33:95-99; 1978.
Emmerson, B.T. Arthritis Rheum. 11:623-634; 1968. (As cited by
Tsuchiya 1979)
Epstein, S.S.; Mantel, N. Carcinogenicity of tetraethyllead. Experienta
24:580-581; 1968. (As cited by WHO 1977)
Eyden, B.P.; Maisin, J.R.; Mattelin, G. Long-term effects of dietary
lead acetate on survival, body weight and seminal cytology in mice.
Bull. Environ. Contain. Toxicol. 19(3) :266-272; 1978.
Fahim, M.D.; £t _al. Effects of subtoxic lead levels on pregnant women
in the state of Missouri. Res. Commun. Chem. Pathol. Pharmacol. 13:309;
1976. (As cited by U.S. EPA 1980)
Fairhall, L.T.; Miller, J.W. A study of the relative toxicity of the
molecular components of lead arsenate. Publ. Health Rep. 56:1610; 1941.
(As cited by IARC 1972)
Ferm, V.H.; Carpenter, S.J. Exp. Mol. Pathol. 7:208; 1967. (As cited
by Earl and Vish 1979)
Fine, B.P.; Jortner, B.S.; Ty, A.; Cause, D.; Lyons, M. The effects of
body burdens of lead on the growing rat kidney. Environ. Res. 19:215-
220; 1979.
Gale, T. A variable emfaryotoxic response to lead in different strains
of hamsters. Environ. Res. 17(3):325-333; 1978.
Gerber, G.; Maes, J.; Deroo, J. Effect of dietary lead on placental
blood flow and on fetal uptake of alpha-amino isobutyrate. Arch.
Toxicol. 41(2):125-131; 1978.
Gilani, S.H. Congenital anomalies in lead poisoning. Pathol. Microbiol.
39:85; 1973. (As cited by Damstra 1977)
Gilsinn, J.F. National Bureau of Standards Technical Note No. 746.
Gaithersburg, MD: National Bureau of Standards; 1972. (As cited by
Mahaffey 1978)
5-44
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I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Hayakawa, K. Microdetermination and dynamic aspects of in vivo alkyl-
I lead compounds in vivo. Part II. Studies on the dynamic aspects of
alkyllead compounds in vivo. Jap. J. Hyg. 26:526; 1972. (As cited by
GrandieAn anA Miale^n lOTO-v "*
I
I
Goldwater, L.J.; Hoover, A.W. An international study of "normal" levels
of lead in blood and urine. Arch. Environ. Health 15:60: 1967. (As
cited by Posner 1977)
Goyer, R.A. Effect of toxic, chemical and environmental factors on the
kidney. Monogr. Pathol. 20:202-217; 1979.
Goyer, R.A.; Mushak, P. Lead toxicity laboratory aspects. Adv. Mod
Toxicol. 2:41-77; 1977.
Goyer, R.A.; Rhyne, B.C. Pathological effects. Int. Rev. Exp. Pathol
12:1-77; 1973. (As cited by U.S. EPA 1977)
Goyer, R.A.; Tsuchiya, K.; Leonard, D.L.; Kahyo, H. Aminoaciduria in
Japanese workers in the lead and cadmium industries. Am. J. din
Pathol. 57:635-642; 1972. (As cited by WHO 1977)
Grandjean, P.; Nielsen, T. Organolead compounds: environmental health
aspects. Residue Rev. 72:97-148; 1979.
Granick, J.L.; Sassa, S.; Kappas, A. Some biochemical and clinical
aspects of lead intoxication. Adv. Clin. Chem. 20:287-339; 1978.
Gray, L.E.; Reiter, L.W. Lead-induced developmental and behavioral
changes in the mouse. Presented at the 16th annual meeting society of
toxicology, Toronto, Canada; March 1977. (As cited by U.S. EPA 1977)
Greathouse, D.; Craun, G.F.; Worth, D. Epidemiological study of the
relationship between lead drinking water and blood lead levels
Proceedings of the 10th annual meeting on trace metals in the environ-
ment. Columbia, MO: University of Missouri Press; 1976: 305-309
(As cited by Mahaffey 1978)
Gross, S.B. Oral and inhalation lead exposures in human subjects.
New York, NY: Lead Industries Association, Inc.; 1979. 71 p.
Hackett, P.L.; Hess, J.O.; Sikov, M.R. Lead distribution and effects
during development in the rat. Developmental toxicology of energy-
related pollutants. U.S. Department of Energy, DOE 47; 1978: 505-519.
im97-2lI;Bi977XP°SUre °f hUmSnS t0 lead> ***' ReV' Pharmaco1' Toxicol.
Harding, F. Metal contaminants in milk and milk products: lead
Bull. Int. Dairy Fed. 105:27-32; 1978.
Grandjean and Nielsen 1979)
5-45
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Hernberg, S.; et _al. Nonrandom shortening of red cell survival times
in men exposed to lead. Environ. Res. 1:247; 1967. (As cited bv
U.S. EPA 1980) y
Hilderbrand, O.C.; et al. Effect of lead acetate on reproduction. Amer
J. Obst. Gynecol. 115:1058; 1973. (As cited by Damstra 1977)
Hinton, D.E.; Lipsky, M.M.; Heatfield, B.M.; Trump, B.F. Opposite
effects of lead on chemical carcinogenesis in kidney and liver of rats.
Bull. Environ. Contam. Toxicol. 23(4-5) -.464-469; 1979.
International Agency for Research on Cancer (IARC). IARC Monographs on
the evaluation of the carcinogenic risk of chemical to man. 1:40-50-
1972.
Karalekas, P.C.; Craun, G.F.; Hammonds, A.F.; Ryan, C.R.; Worth, D.J.
Lead and other trace materials in drinking water in the Boston metropoli-
tan area. J. New Engl. Waterworks Assoc. 90:150-172; 1976.
Karalekas, P.C.; Ryan, C.R.; Larson, C.D.; Taylor, F.B. Alternative
methods for controlling the corrosion of lead pipe. Journal NEWWA
92(2):159-178; 1978.
Kazantzis, G.; Lilly, L.J. Mutagenic and carcinogenic effects of metals.
Handbook on the toxicology of metals. Friberg, L. ; Nordberg, G.G.:
Vouk, V.B. (eds). New York, NY: Elsevier/North-Holland Biomedical
Press; 1979: 241-272.
Kehoe, R.A. The metabolism of lead in health and disease. The Harben
Lectures, 1960. J. Rev. Inst. Publ. Health Hyg. 24:81-96, 101-1?0
129-143, 177-203; 1961. (As cited by WHO 1977) " '
Kennedy, G.L.; Arnold, D.W.; Calandra, J.C. Teratogenic evaluation of
lead compounds in mice and rats. Fd. Cosmet. Toxicol. 13:629; 1975.
(As cited by Grandjean and Nielsen 1979)
Keppler, J.F.; .et .al. Interlaboratory evaluation of the reliability of
blood lead analysis. Am. Ind. Hyg. Assoc. J. 31:412; 1970. (As cited
by Kolbye et al. 1974)
Kerin, Z. Tagliche gleiaufnahme mit der bauernkost aus dem emissiongebiet
einer bleihutte. Protectio vitae 71:22-23; 1972. (As cited by WHO 1977)
Kimmel, C.A.; Grant, L.D.; Sloan, C.S. Chronic lead exposure: assess-
ment of developmental toxicity. Teratol. 13:27A; 1976. (As cited by
U.S. EPA 1977)
Kimmel, C.A.; Grant, L.D.; Sloan, C.S.: Gladen, B.C. Chronic low-level
lead toxicity in the rat. Toxicol. Appl. Pharmacol. 56:28-41; 1980.
5-46
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
King, B.C. Maximum daily intake of lead without excessive body lead-
burden in children. Amer. J. Dis. Child 122:337-340; 1971.
Kobayashi, N.; Okamoto, T. Effects of lead oxide on the induction of
lung tumors in Syrian hamsters. J. Nat. Cancer Inst. 52(5):1605-1610;
1974. (As cited by WHO 1977 and U.S. EPA 1977)
Kolbye, A.C.; Mahaffey, K.R.; Fiorino, J.A.; Cornellussen, P.C.;
Jelinek, C.F. Food exposures to lead. Environ. Health Persp. 7(Exp.):
65-74; 1974.
Kotok, D. Development of children with elevated blood levels: A con-
trolled study. J. Pediatr. 80:57; 1972. (As cited by U.S. EPA 1980)
Krasovskii, G.N.; Vasukovich, L.Y.; Chariev, O.G. Experimental study
of biological effects of leads and aluminum following oral administra-
tion. Environ. Health Persp. 30:47-51; 1979.
Krigman, M.R. Neuropathology of heavy metal intoxication. Environ.
Health Persp. 26:117-120; 1978.
Lancranjan, I.; et al. Reproductive ability of workmen occupationally
exposed to lead. Arch. Environ. Health 30:396; 1975. (As cited by
U.S. EPA 1980)
Landrigan, P.J.; Baker, E.L. Increased lead absorption with aremia
and slowed nerve conduction in children near a lead smelter. Pediatrics
89:904; 1976. (As cited in U.S. EPA 1980)
Landrigan, P.J.; Gehlbach, S.H.; Rosenblum, B.F.; Shoults, J.M.;
Candelaria, R.M.; Barthel, W.F.; Liddle, J.A.; Smrek, A.L.; Staehling,
N.W. ; Sanders, J.D.F. Epidemic lead absorption near an ore smelter:
The role of particulate lead. New Engl. J. Med. 292:123-129; 1975.
(As cited by U.S. EPA 1977)
Lane, R.E. The care of the lead worker. Br. J. Ind. Med. 6:1243; 1949.
(As cited by U.S. EPA 1980)
Lansdown, R.G.; .et .al. Blood-lead levels, behavior and intelligence.
A population study. Lancet 1:1166; 1974. (As cited by U.S. EPA 1980)
Laporte, R.E.; Talbott, E.E. Effects of low levels of lead exposure on
cognitive function: A review. Arch. Environ. Health 33(5):236-239;
1978.
Leonard, A.; Linden, G.; Gerber, G.B. International symposium on
environmental health aspects (lead); 1972 October 2-6, Amsterdam, the
Netherlands, Euratom Publications; 1973: 303-309. (As cited by
Kazantzis and Lilly 1979)
5-47
-------
Lepow, M.L.; Bruckman, L.; Rubino, R.A.; Markowitz, S.; Gillette, M.;
Kapish, J. Role of airborne lead in increased body burden of lead in
Hartford children. Environ. Health Persp. 7(Exp.):99-102; 1974.
Levander, O.A. Lead toxicity and nutritional deficiencies. Environ.
Health Persp. 29:115-125; 1979.
Lilis, R.; et al. Lead effects among secondary lead smelter workers
with blood levels below 80 yg/1100 ml. Arch. Environ. Health, p. 256;
1977. (As cited by U.S. EPA 1980).
Lilis, R.; Valciukas, J.; Fischbein, A.; Andrews, G.; Selikoff, I.J.;
Blumberg, W. Renal function impairment in secondary lead smelter
workers; correlations with zinc protoporphyrin and blood lead levels.
J. Environ. Path. Toxicol. 2:1447-1474; 1979.
Lin-Fu, J.S. In: Proceedings of the international conference on heavy
metals in the environment, Toronto, 27-31 October 1975. Electric Power
Research Institute (Calif.), EPA, Institute for Environmental Studies
(University of Toronto), International Nickel Company of Canada Ltd.,
National Institute of Occupational Safety and Health (Cincinnati),
National Research Council of Canada, SCOPE, WHO; 1976. (As cited by
Tsuchiya 1979)
Mahaffey, K.R. Dietary lead intake of children living in Washington, DC.
Unpublished data. [1976]. (As cited by Mahaffey 1978)
Mahaffey, K.R. Quantities of lead producing health effects in humans:
_sources and bioavailability. Environ. Health Persp. 19:285-295; 1977.
Mahaffey, K.R. Environmental Exposure to lead. Nriagu, J.D. ed. The
biogeochemistry of lead in the environment. New York, NY: Elsevier/
North-Holland Biomedical Press; 1978: Chapter 11, 1-36.
Maisin, J.R.; Jade, J.M.; Lambiet-Collier, M. Progress report on
morphological studies of the toxic effects of lead on the reproductive
organs and the embryos. Economic Community of Europe Contract No.
080-74-7, Env. B.; Belgium, 1975. (As cited by U.S. EPA 1977).
Mao, P.; Molnar, J.J. The fine structure and histochemistry of lead-
induced renal tumors in rats. Amer. J. Path. 50:571; 1967. (As cited
by IARC 1972)
McCabe, E.B. Age and sensitivity to lead toxicity: a review. Environ.
Health Persp. 29:29-33; 1979.
McClain, R.M.; Becker, B.A. Teratogenicity, fetal toxicity and placental
transfer of lead nitrate in rats. Toxicol. Appl. Pharmacol. 31:72-82;
1975>
5-48
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
McFeatters, A. Lead. The Columbus Citizen-Journal 17(56, Sect. 2):11;
1976. (As cited by Bell _et al. 1979)
McLaughlin, M.; Stopps, G.J. Smoking and lead. Arch. Environ. Health
26:131; 1973. (As cited by Posner 1977)
McLaughlin, J.; Marliac, J.P.; Verrett, M.J.; _et _al. Toxicol. Appl.
Pharmacol. 5:760-711; 1963. (As cited by Rosen and Sorell 1978)
McNeil, J.L.; £t _al. Evaluation of long-term effects of elevated blood
lead concentrations in asymptomatic children. Arhiv. Rig. Rada. Toksikol.
14:97; 1975. (As cited by U.S. EPA 1980)
Mitchell, D.G.; Aldous, K.M. Lead content of foodstuffs. Environ.
Health Persp. 7(Exp.):59-64; 1974.
Momcilovic, B. The effect of maternal dose or lead retention in suckling
rats. Arch. Environ. Health 33(3):115-117; 1978.
Momcilovic, B. Lead metabolism in lactation. Experientia 35(4):517-518•
1979.
Moore, M.R. Diet and lead toxicity. Proc. Nutr. Soc. 38:243-250; 1979.
Moore, M.R.; Meredith, P.A.; Campbell, B.C.; Goldberg, A.; Pocock, S.J.
Contribution of lead in drinking water to blood-lead. Lancet 11(8039):
661-662; 1977.
Moore, M.R.; Meredith, P.A. The carcinogenicity of lead. Arch. Toxicol.
42(2):87-94; 1979.
Moore, M.R.; Meredith, P.A.; Watson, W.S.; Sumner, D.J.; Taylor, M.K.;
Goldberg, A. The percutaneous absorption of lead-203 in humans from
cosmetic preparations containing lead acetate, as assessed by whole-body
counting and other techniques. Fd. Cosmet. Toxicol. 18:399-405; 1980.
Muir, W.; Bridbord, K. Lead and women, a unique problem? Review of
lead toxicity. Proceedings conference on women and the workplace; 1976
June 17-19. Soc. Occup. Environ. Health pp. 227-231; 1977.
Muro, L.A.; Goyer, J.R.A. Arch. Pathol. 87:660-663; 1969. (As cited by
Kazantzis and Lilly 1979).
Mykkanen, H.M.; Dickerson, J.W.T.; Lancaster, M. Strain differences in
lead intoxication in rats. Toxicol. Appl. Pharmacol. 52:414-421; 1980.
National Research Council (NRC); 1980. (As cited in Food Chem. News.
pp. 53-56; March 24, 1980).
5-49
-------
Needleman, H.L. ed. Low level lead exposure, the clinical implications
of current research. New York, NY: Raven Press; 1980.
Needleman, H.L.; Davidson, I.; Sewell, E.M. ; Shapiro, D.M. New Engl.
J. Med. 290:245-248; 1974. (As cited by Rosen and Sorell 1978)
Needleman, H.L. ; Gunnoe, C. ; Leviton, A. ; Reed, R. ; Peresie, H. ;
Maher, C. ; Barrett, P. Deficits in psychologic and classroom perfor-
mance of children with elevated dentine lead levels. New Engl. J. Med.,
300:689-695; 1979.
Nelson, W.C.; ££. jj.. Mortality among orchard workers exposed to lead
arsenate spray: a cohort study. J. Chron. Dis. 26:105; 1973. (As
cited by U.S. EPA 1980)
Neshkov, N.S. Effects of chronic poisoning with ethylated gasoline on
spermatogenesis and sexual function in males. Gig. Truda i Prof. Zabol.
15:45; 1971. (As cited by Grandjean and Nielsen 1979)
Nielsen, T. ; et. al.. Unpublished results; 1979. (As cited by Grandjean
and Nielsen 1979)
Nogaki, K. On action of lead on body of lead refinery workers: parti-
cularly conception, pregnancy and parturition in case of females and
their newborn. Excerp. Med. (XVII) 4:2176; 1958. (As cited by U.S. EPA
1977)
Nordman, C.H. ; Hernberg, S. Blood lead levels and erythrocyte d-amino
levulinic acid dehydratase activity of selected population groups in
Helsinki. Scand. J. Work. Environ. Health 1:210-232; 1975. (As cited
by WHO 1977)
Nriagu, J. ed. The biogeochemistry of lead in the environment. New
York, NY: Elsevier/North Holland Biomedical Press; 1978.
Nriagu, J. ed. The biogechemistry of lead in the environment. Part B.
Biological effects. New York, NY: Elsevier/North-Holland Biomedical
Press; 1978.
Obe, G. ; Beek, B. ; Dudin, G. Some experiments on the action of lead
acetate on human leukocytes in vitro. Mutat. Res. 29:283; 1975.
O'Brien, J. Lead in Boston water: its cause and prevention. Journal
NEWWA 90:173-180; 1976.
Odenbro, A.; Kihlstrom, J.E. Frequency of pregnancy and ova implantation
in triethyl lead-treated mice. Toxicol. Appl Pharmacol. 39:359; 1977.
(As cited by Grandjean and Nielsen 1979)
O'Riordan, M.L.; Evans, H.J. Absence of significant chromosome damage
in males occupationally exposed to lead. Nature 247:50-53; 1974. (As
cited by WHO 1977)
5-50
-------
I
I
I
I
I
I
I
I
1
I
I
I
I
I
I
I
I
I
I
Oyasu, R.; Battifora, H.A.; Clasen, R.A.; McDonald, J.H.; Mass, G.M.
Induction of cerebral gliomas in rats with dietary lead subacetate and
2-acetylaminofluorene. Cancer Res. 30:1248; 1970. (As cited by IARC
1972)
Palmisano, P.A.; Sneed, R.C.; Cassady, G. Untaxed whiskey and fetal
lead exposure. J. Pediatr. 75:869; 1969. (As cited by WHO 1977)
Panova, Z. Early changes in the ovarian function of women in occupa-
tional contact with inorganic lead. Works United Res. Inst. Hyg. Ind.
Saf. 23:161-166; 1972. (As cited by WHO 1977)
Patterson, J.W.; O'Brien, J.E. Control of lead corrosion. Journal
AWWA 71 (5):264-271; 1979.
Payne, B.J.; Saunders, L.Z. Heavy metal nephropathy of rodents. Vet.
Path. 15(5):51-86; 1978.
Perino, J.; Ernhart, C.B. The relation of subclinical lead level to
cognitive and sensorimotor impairment in black preschoolers. J. Learn.
Dis. 7:26; 1974. (As cited by U.S. EPA 1980)
Posner, H.S. Indexes of potential lead hazard. Environ. Health Persp.
19:261-284; 1977.
Pueschel, S.M.; Kopitao, L.; Schwachman, H. A screening and follow up
study of children with an increased lead burden. J. Am. Med. Assoc.
333:462-466; 1972. (As cited by WHO 1977)
Rabinowitz, M.B. Lead contamination of the biosphere by human activity,
Los Angeles, CA: University of California at Los Angeles; 1974. Dis-
sertation. (As cited by U.S. EPA 1977)
Rabinowitz, M.B.; Wetherill, G.W.; Kopple, J.D. Lead metabolism in the
normal human: stable isotope studies. Science 182:725-772; 1973.
(As cited by WHO 1977)
Rabinowitz, M.B.; Wetherill, G.W.; Kopple, J.D. Studies of human lead
metabolism by use of stable isotope tracers. Environ. Health Persp.
Exp. 7:145-166; 1974. (As cited by WHO 1977)
Rabinowitz, M.B.; Wetherill, G.W.; Kopple, J.D. Kinetic analysis of
lead metabolism in healthy humans. J. Clin. Invest. 58:260; 1976. (As
cited by Posner 1977)
Ramel, C. The effect of metal compounds on chromosome segregation.
Mutat. Res. 21:45; 1973. (As cited by Grandjean and Nielsen 1979)
Reiter, L.W.; Anderson, G.E.; Laskey, J.L.; Cahill, D.F. Developmental
and behavioral changes in the rat during chronic exposure to lead.
Environ. Health Persp. 12:119-123; 1975. (As cited by U.S. EPA 1977)
5-51
-------
Repko, J.D.; Corum, C.R. Critical review and evaluation of the neuro-
logical and behavioral sequelae of inorganic lead absorption. CRC Grit
Rev. Toxicol. 6(2) :135-187; 1979.
Roberts, T.M. ; Hutchinson, T.C. ; Paciga, J. ; Chattopadhyay, A.;
Jervis, R.E. ; Van Loon, J. ; Parkinson, D.K. Lead contamination around
secondary smelters: estimation of dispersal and accumulation bv humans.
Science 186(4169) : 1120-1123; 1974.
Robinson, M.J. ; Karpinski, F.E., Jr.; Brieger, H. The concentration of
lead in plasma, whole blood and erythrocytes of infants and children.
Pediatrics 21:793; 1958. (As cited by Posner 1977)
Robinson, T.R. 20-year mortality of tetraethyl lead workers. J. Occup.
Med. 16:601; 1974. (As cited by Grandjean and Nielsen 1979)
Roels, H.A. ; Buchet, J.P. ; Bernard, A.; Hubermont, G. ; Lauwerys , R.R. ;
Masson, P. Investigations of factors influencing exposure and response
to lead, mercury, and cadmium in man and animals. Env. Health Persp .
25:91-96; 1978.
Rosen, J.F.; Sorell, M. The metabolism and subclinical effects of lead
in children. The biogeochemistry of lead in the environment, Part b.
Biological effects. Nriagu, J.D. ed. New York, NY: Elsevier/North-
Holland Biomedical Press; 1978: 151-172,
Sandhu, S.S.; Warren, W. J. ; Nelson, P. Inorganic contaminants in rural
drinking waters. Journal AWWA 69(4) :219-222; 1977.
Sandstead, H.H.; Michalakis , A.M.; Temple, T.E. Lead intoxication. Its
effect on the renin aldosterone response to sodium deprivation. Arch.
Environ. Health 20:356-363; 1970. (As cited by Mahaffey 1978)
Schmid, E. ; Bauchinger, M. ; Pietruck, S. ; Han, G. Die cytogenetische
wirkung von Blei in menschlichen peripheren lymphocyten ±n vitro and ±n
vivo* Mutat. Res. 16:401-406; 1972. (As cited by U.S. EPA 1977)
Schwanitz, G. ; Lehnert, G. ; Gebhart, E. Desch. Med. Wochenschr 95:1636-
1641; 1970. (As cited by Kazant2is and Lilly 1979)
Settle, D. ; Patterson, C. Lead in albacore: guide to lead pollution
in Americans. Science 207:1167-1176; 1980.
Shih, T.-M. ; Hanin, I. Chronic lead exposure in immature animals: neuro-
chemical correlates. Life Sci. 23(9) :877-888; 1978.
Six, K.M. ; Goyer, R.A. The influence of iron deficiency on tissue content
and toxicity of ingested lead in the rat. J. Lab. Clin. Med. 79:128-136;
1972. (As cited by WHO 1977)
5-52
-------
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
I
Stewart, R.A.; Skeberdis, J. Lead intake of United States infants.
Gerber Research Center, Fremont, Michigan. Unpublished data; 1975.
(As cited by Mahaffey 1978)
Taylor, F.B. Overview of New England water supply problems. J. N.E.
Water Works Assoc. 91(2):165-174; 1977.
Tepper, L.B. Arch. Environ. Health 7:76-85; 1963. (As cited by Tsuchiya
1979)
Tepper, L.B.; King, B.C. Maximal daily intake of lead without excessive
body lead-burden in children. Am. J. Dis. Child. 122:337; 1971. (As
cited by Mahaffey 1978)
Tepper, L.B.; Levin, L.S. A survey of air and population lead levels in
selected American communities. Final report. Seven cities study.
Cincinnati, OH: University of Cincinnati, College of Medicine; 1972.
(As cited by Bell .et al. 1979)
Tola, S.; Hernberg, S.; Asp, S.; Nikkanen, J. Parameters indicative of
absorption and biological effect in new lead exposure. A prospective
study. Brit. J. Ind. Med. 30:134-141; 1973. (As cited by WHO 1977)
Tsuchiya, K. Lead. Friberg, L.; Nordberg, G.F.; Vouk, V.B. eds.
Handbook on the toxicology of metals. New York, NY: Elsevier/North-
Holland Biomedical Press; 1979: 451-484.
U.S. Department of Health, Education and Welfare (U.S. DHEW). Community
water supply study. Analysis of national survey findings. Washington,
DC: Bureau of Water Hygiene, Environmental Health Service: 1970. Ill p.
U.S. Environmental Protection Agency (U.S. EPA). Air quality criteria
for lead. Washington, DC: Office of Research and Development, U.S.
Environmental Protection Agency; 1977. Available from NTIS; PB 28 0411.
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for lead. Report No. EPA 440/5-80-057. Washington, DC:
Criteria and Standards Division, Office of Water Regulations and
Standards; 1980.
Van Esch, G.J.; Van Gendersen, H.; Wink, H.H. The induction of renal
tumors by feeding of basic lead acetate to rats. Brit. J. Cancer 16:289-
1962. (As cited by LARC 1972)
Van Esch, G.J.; Kroes, R. The induction of renal tumors by feeding basic
lead acetate to mice and hamsters. Brit. J. Cancer 23:765; 1969. (As
cited by LARC 1972)
Vurdelja, N.; Farago, F.; Nikolie, V.; Vuckovic, S. Clinical experiences
with intoxications of fuel containing lead-tetraethyl. Folia Facultatis
Medical Univ. Comenianae 5:133; 1967. (As cited by Grandjean and Nielsen
1979)
5-53
-------
Walker, B. Lead content of milk in infant formula. J. Food Protection
43(3):178-179; 1980.
Walter, S.D.; Yankel, A.J.; von Lindern, I.H. Age-specific risk factors
for lead absorption in children. Arch. Environ. Health 35(l):53-58; 1980.
Weeden, R.P.; _et al. Occupational lead nephropathy. Am. J. Med. 59:630;
1975. (As cited by U.S. EPA 1980)
Wibberley, D.J.; et al. Lead levels in human placentas from normal and
malformed births. J. Med.-Genetics 14:339; 1977. (As cited by U.S. EPA
1980)
Wigle, D.T.; Charlebois, E.J. Electric kettles as a source of human
lead exposure. Arch. Environ. Health 33:72-78; 1978.
World Health Organization (WHO). Environmental health criteria 3: lead.
New York, NY: The World Health Organization; 1977. 160 p.
Zawirska, B.; Medras, K. Tumours and disorders of the porphyrin metabo-
lism in rats with chronic experimental lead poisoning. I. Morphologic
studies. Zbl. allg. Path. path. Anat. 111:1; 1968. (As cited by IARC
1972)
Zielhuis, R.L. Int. Arch. Occup. Environ. Health 35:1-18, 19-35; 1975.
(As cited in Tsuchiya 1979)
Zielhuis, R.L.; Wibowo, A.A.E. Review paper: susceptibility of adult
females to lead: effects on reproductive function in females and males.
2nd international workshop on permissible limits for occupational exposure
to lead. In press; 1977. (As cited by U.S. EPA 1977)
Zollinger, H.U. Durch chronische bleivergiftung erzeugte nierenadenome
und carcinoma bei ratten und ihre beziehungen zu den entsprechenden
neubildung des menschen. Virchow Arch. 323:694-710; 1953. (As cited
by Moore and Meredith 1979)
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6.0 BIOTIC EFFECTS AND EXPOSURE
6.1 EFFECTS ON BIOTA
6.1.1 Introduction
This section provides information on the exposure levels of lead
that disrupt the normal behavior and metabolic processes in aquatic and
terrestrial organisms. Data are based on the laboratory studies from
the available literature. In addition to its widespread publicity with
regard to human health effects, lead has been the focus of extensive
research on plant and animal toxicosis. The U.S. EPA (1980) has reviewed
this data, thus only brief discussions will be contained here.
In aquatic bioassays, a certain amount of variability is expected,
owing to several factors. Differences in test type, for example, static,
or continuous flow-through tests, may influence the results. In addition,
water parameters, such as hardness and the presence of other chemicals,
are known to influence the toxicity of lead to various aquatic organisms,
as well as the form of lead (inorganic or organic) used. Thus, variations
in these parameters between experiments could yield varying results.
Other factors include the duration of exposure and species and develop-
mental stage of the test organisms. Because some species and stages may
be more sensitive to lead than others, it is not always appropriate to
compare the results of different studies.
6.1.2 Freshwater Organisms
6.1.2.1 Chronic and Sublethal Effects
When chronically exposed to low levels, aquatic biota may become
acclimated to a toxic substance, or they may exhibit adverse effects,
such as decreased respiration, lack of responsiveness to stimulation,
growth inhibition, and malformation. Even if aquatic fauna are not
killed by long-term exposure to lead, the vigor and diversity of local
populations may still be endangered.
Data on the sublethal effects of lead on freshwater fish are summar-
ized in Table 6-1. The lowest concentration at which effects were
reported was 7.6 ug/1 (hardness 28 mg/1), which caused developmental
irregularities in rainbow trout fingerlings in a chronic exposure test
(Davies et^ a!L. 1976). Other sublethal effects have been noted at lead
concentrations as high as 110 mg/1, and include fin erosion, tail black-
ening, loss of equilibrium, poor resorption of yolk in fry, and growth
inhibition. The U.S. EPA (1980) reported chronic values ranging from
19 yg/1 (hardness 28 mg/1) for the rainbow trout (Salmo gairdneri) to
174 yg/1 (hardness 38 mg/1) for the whtie sucker (Catastomus commersoni).
These values were primarily based on effects observed in early life stages,
6-1
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TAIU.E 6-1. SIIKI.ICTIIAL KKFECTS OF I.KAI) ON KKESllUATtiK K1SII
Species
Kalnbow trout, fingerling
(Salmo galrdnerl)
Zebrafish, eggs
(Brachydanlo rerio)
Goldfish
(Ca raas jus auratus)
Ox
to
Halnbow trout, yearling
(Salmo gatrdnerl)
Brook trout
(Salvellnus fontfnalis)
Chinook salmon
(Oncorhynchus tshawytacha)
Concentration
(mg/1)
0.0076-0.064
0.036-0.072
0.070
6.6
110
0.12
2.4
0.134
10
Compound
Pb (N03)2
Pb (N03)2
Pb (NOp.,
Pb (N03)2
Pb (N03)2
Pb (N03)2
Pb (N03)2
Experimental
Condi t Ions
Life-cycle, 28 &
353 mg/1 hardness
Embryo-larval, 26°
1.6 mg/1 alkalinity
static
pll 6.0-6.9, 23°
soft water
hard water
Flow- through 32 wk,
135 mg/1 hardness,
pll 7.7, 11°
44 mg/1 hardness
Static, 4-6 hour, 11°
pll 7.2, 0-17 mg/1 hard
Effects
I.ordoticollosls, paralysis,
muscular atrophy,
degeneration of caudal fin,
blackening of tall
Poor resorptlon of yolk In
fry, erosion of tall & fin,
spinal curvature, apparent
eplthellomas
Significant Impairment ot
conditioned response
7-day LC50
7-day l.C50
Increase In number of
erythrocytes, 30% Incidence
of black tails
21-day LC50
Reduced growth
Loss of equilibrium
Reference
Uavies et al.
(1976)"
Ozoh (1979a)
Uelr and Nine
(1970)
Hudson et al.
(1978)
Christensen
(1975)
MacPhee and
Reulle (1969)
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The range of sublethal and chronic effect concentrations for inver-
tebrates seems considerably narrower than for fish (see Table 6-2),
although this could be a function of the particular species tested. The
isopod, Asellus meridianus, exhibited reduced growth rates in 0.1 mg/1
lead over a period of 20 days (Brown 1976). The only other reported
sublethal effect was reduced respiration in the sludgeworm, which was
attributed to the mucous-metal complex that formed on the body wall and
blocked the exchange of oxygen and carbon dioxide (Whitley 1968). The
U.S. EPA (1980) reported chronic values ranging from 12 ug/1 to 128 ug/1
for Daphnia maana at water hardness of 52-151 mg/1 CaC03- The chronic
value for the snail (Lymnea palustris) was 25 ug/1 at 139 mg/1 hardness.
These were based on life cycle or partial life cycle tests.
6.1.2.2 Acute Toxicity
Acute toxicity is defined as toxicant-induced mortality over a
short period, generally within 96 hours. Although fish in natural water-
ways are more likely to be exposed to lower concentrations that might
result in chronic or sublethal effects, industrial discharges and spills
can temporarily result in lead levels high enough to cause fish kills.
Some of the acute toxicity data for freshwater fauna are summarized
in Table 6-3. The lowest LC5Q value reported in the literature for a
freshwater fish was 0.3 mg/1 for the three-spined stickleback (Jones
1938). With respect to the intra- and interspecies differences, the
LC5Q values given were derived under a variety of conditions. Such
factors as exposure period (varying between 24 and 96 hours), age of test
organisms, differences in certain water parameters, and bioassay type
(static or flow-through) may account for some of the variation in reported
LC5Q concentrations. For example, values for the bluegill sunfish alone
varied from 23.8 mg/1 to 442 mg/1; apparently the variation was largely
because of the differences in water hardness. Factors contributing to
variability in lead toxicity and fish sensitivity are discussed in greater
detail in Section 6.1.4.
The observed LC5QS for freshwater invertebrates range from 0.124 mg/1
for the scud to 71.0 mg/1 for the snail. The data are insufficient to
determine the relationship between water hardness and lead toxicity for
the species studied.
Other freshwater toxicity data observed mortality in adult leopard
frogs (Rana pipiens) after a 30-day exposure to 100 Ug/1 lead nitrate
(Kaplan et al. 1967).
6.1.2.3 Effects on Microflora
The toxic effects of lead have been observed in a variety of alga,
diatom, and desmid species. Effects similar to those causing sublethal
effects in fish have been observed in short-term bioassays at concentra-
tions ranging from 50 ug/1 to 28.0 mg/1 (U.S. EPA 1980).
6-3
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TABLE 6-2. CIIKONIC AND SWILKTIIAL EKKECTS OK LEAD ON PKESHWATKK INVERTEBRATES
Species
Daplmia Ma^na
Snail
( Lymnea palustrla)
Isopod
(Asellus mcridlanus)
Daphnia niagna
Daphnia magna
Daphnia magna
ON
Crayfish
(Orconectes virilia)
Sludgeworms
(Tubifex tub if ex)
(Limnodrlius hof fmelsteri)
Mayfly
(Ephemcrella grandla)
Concentration Compound
(rag/1)
0.012 Pb(N03)2
0.025 Pb(N03)2
0.1 ?
0.119 l'b(NOj)
0.128 Pb(N03)2
0.3 ?
0.5-2.0 PbAc
1.0- >60 Pb (N03)
3.5 I
Experimental
Conditions
52 mg/1 hardness, life cycle
139 mg/1 hardness, life cycle
25 mg/l hardness, static
20 diws, |.H 7.7
102 mg/1 hardness, life
151 nig/l hardness, life cycle
43 mg/1 hardness
21 days exposure
40 days exposure
pll 6.5-9.5
50 mg/1 hardness
14 days, nil 7. 1
Effects
Chronic value
Chronic value
Reduced growth
Chronic value
Chronic value
LC50
02 consumption slightly
reduced compared w/controls
Decrease In respiration rate
'•C50
Reference
U.S. EPA (1980)
U.S. EPA (1980)
Brown (1976)
U.S. EPA (1980)
U.S. EPA (1980)
Biesinger and
Christensen 91972)
Anderson (1978)
Will t ley (|y6H),
Whit Icy and Sikora
(1970)
Nehriny (1976)
(Ephemerella grandls)
Stonefly
(Pteronarcys californica)
Caddisfly
(Hydropsyche bettenl)
Insect
(Acroneuria lycorias)
16.0
>19.2
32.0
hf. n
PbSO,
44 rag/1 hardness
7 days, static
50 mg/1 hardness
14 days exposure
44 rng/1 hardness
7 days, static
44 mg/1 hardness
14 days, static
l'C
50
LC
50
LC
50
Warnick and Bull
(1969)
Nehriii,; (1976)
Warnick and Bell
(1969)
Warnick and Bell
(1969)
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TABLE 6-3. ACUTE TOXICITY (LC5Q) OF LEAD TO FRESHWATER FAUNA
Species
Concentration
Ranee
Range of Hardness
Three-spined stickeback (Gasterosteus
aculeatus)
Rainbow trout (Salmo gairdneri)
Fathead minnow (Pimephales protnelas)
Brook trout (Salvelinus fontinalis)
Guppy (Poecilia reticulata)
Bluegill sunf ish (Lepomis macrochirus)
Goldfish (Carassius auratus)
Mosquitofish (Gambusia affinis)
Red shiner (Notropis lutrensis)
(mg/1)
0.3a
1.17-542.0
2.4 -482.0
4.1
20.6
23.8-442.0
31.5
240.0
630.0
(mg/1 as CaC03)
9
28-353
20-360
44
20
20-360
20
20
9
Invertebrates
Scud (Gammarus pseudolimnaeus)
Isopod (Asellus meridianus)
Daphnia magna
Daphnia hyalina
Copepod (Eudiaptomus padanus)
Copepod (Cyclops abyssorum)
Snail (Lymnaea emarginata)
Sludgeworm (Tub ifex tubifex)
Rotifer (Philodina acuticornis)
Snail (Goniobasis livescens)
0.124°
0.28
0.45-1.91
0.60
4.0
5.5
14.0
27.5-49.0
40.8
71.0
Jones (1938).
'Spehar et al. (1978).
Source: U.S. EPA (1980), except as otherwise noted.
6-5
44-48
25
45-152
66
66
66
154
?
25
154
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6.1.3 Marine Organisms
Information on lead toxicosis in marine finfish is limited to two
Mof ' aUd Tly °nS aCUte toxiclty st^y was available. Weis and Weis
(1976) exposed mummichog (Fundulus heteroclitus) with partially amputated
caudal fins to various lead nitrate solutions to determine the effect of
lead on fin regeneration. A concentration of 0.1 mg/1 was found to
stimulate fin growth, while 1.0 mg/1 lead significantly inhibited
regeneration.
and co-workers (1926) observed growth inhibition in juvenile
plaice (Pleuronectes £latessa) exposed to 2 mg/1 colloidal lead as Pb*
So!2! ,TlT\ 197?) rep°rted a 96-hour LC50 of 315 mg/1 for the mummi-
chog in static bioassays.
Suble Sfl6fd t°XfCityJ^ marinS invert^rates are much more abundant
ln 6
rate whh v Kn 6 larVal devel°P™^ and reduced growth
beSn observed in concentrations as low as 50 u./i in the
TP PanuP6US arSii) (BeniJ^-daus and Benijts 1975)
with ?5° ValUSS haVe beSn rep°rted in the "nge of 1.0-30.0 m*/l
Information on acute toxicity is summarized in Table 6-4 The
lowest reported LC50 is 0.72 mg/1 for the hardshell clam larvae.
6o1*4 Factors Affecting the Aquatic Toxicity of Lead
Numerous variables in a natural aquatic environment influence the
availability and toxicity of lead to biota. The hardness of the water
dissolved solids, . oxygen content, pH, and interactions between heavy '
metals modify the toxicity of lead to varying degrees.
Among these parameters, water hardness appears to be the most
significant. The negative correlation between lead toxicity and hard-
ness has been confirmed in numerous laboratory studies. The most illus-
trative example of this relationship is found in the results of a study
by Pickering and Henderson (1966). In static bioassays on fathead minnows
in water with either 20 mg/1 or 360 mg/1 hardness, the authors calculated
96-hour LC50s of 5.58 mg/1 and 482.0 mg/1 lead, respectively. Similar
results were obtained in experiments with the bluegill. Davies et al.
(1976) found that the 96-hour LCso for rainbow trout varied by a factor
of >400 in a water hardness range of 28-353 mg/1; however, tests in soft
water were flow- through, while those in hard water were static. Miller
and Landesman (1978) reported that magnesium ions (component of
water hardness) have suppressive effects on the toxicity of lead to frog
(Xenopus sp.) embryos.
The presence of other dissolved solids may also alter the toxicity
of lead to aquatic organisms. Wong et al. (1978) recommend the use of
6-6
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1
1
1
1
•
1
1
1
1
1
1
1
1
•
1
1
1
1
TABLE 6-4. ACUTE TOXICITY (LC50) OF LEAD
Sjaecies ^50 Concentration
(mg/1)
Hard-shell clam, larvae 0.72-0.80
(Mercenaria mercenaria)
Polychaete, trochophore 1.2
(Capltella cap it at a)
Eastern oyster, larvae 2.2 - 3.6
(Crassostrea virginica)
Isopod 10a
(Jaera albifrons)
Isopod 10a
(Jaera nordmanni)
Softshell clam 27.0
(Mya arenaria)
K
Prawn 375
(Pandalus montagui)
K
Cockle >500
(Cardium edule)
aJones (1975).
b
Portmann and Wilson (1971) .
Source: U.S. EPA (1980), except as otherwise
6-7
TO MARINE INVERTEBRATES
Experimental
Conditions
Static, nominal,
48 hours
Static, nominal,
96 hours
Static, nominal,
48 hours
Static, 24 hours,
5°C, 1% seawater
Static, 36 hours,
5°C, 1% seawater
Static, nominal, 96 hours,
salinity 30° /oo, pH 7.95
Static, renewal,
48 hours, 15° C
Static, renewal,
48 hours, 15 °C
noted.
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phosphate-free conditions in laboratory bioassays on algae, because
phosphates also decrease lead toxicity. The assessment of Dorfman (1977)
on the influence of varying salinity on lead toxicity to the mummichog
proved inconclusive.
In natural waters, lead occurs in free ionic forms, in complexed
forms with organic and inorganic molecules, and in association with
particulate matter (Wong j2t_ al^. 1978) (see Section 4.3). The consensus
of the literature surveyed is that the free ion, with the exception of
certain organolead compounds, is the form of lead most often associated
with toxicity. Davies et al. (1976) found that when lead was added to
hard water, precipitates of lead salts were formed, probably as carbon-
ates and hydroxides. Such precipitates (in addition to chelates, organic
complexes, and lead absorbed to particulates) are apparently less avail-
able to aquatic organisms for uptake and metabolism. Barber and Ryther
(1969) found that the addition of the chelating agent ethylenediamine-
tetraacetic acid (EDTA) decreased or completely masked lead toxicity.
On the other hand, small amounts of lead may be methylated to more avail-
able forms in sediments, the amounts produced are probably too small to
contribute significantly to overall aquatic lead toxicity.
In the case of water hardness, Zitco (1976) has suggested another
mechanism for lead toxicity suppression. Base metals, such as calcium
or magnesium, might compete with heavy metals, such as lead, for active
sites on the surface membranes of organisms. In hard water, the concen-
trations of these metals would be greater than lead, and any such sites
would quickly be saturated, and hence unavailable to lead. Matthiesson
and Brafield (1977) have suggested that the base metals may protect the
biochemical processes with which zinc interferes; this hypothesis could
also be applied to lead, assuming certain similar characteristics between
the two heavy metals.
Dissolved oxygen level and pH are two parameters that are normally
controlled in laboratory studies. In a static bioassay on rainbow trout,
Lloyd (1961) found that the toxicity of lead increased with a decrease
in oxygen concentration. Tubificid worms were more sensitive to lead at
pHs of 6.5 and 8.5, even though they showed more resistance at pH 7.5
(Whitley 1968). In both cases, the direct effects of these parameters
may have lowered the organisms' tolerance to lead. However, the toxicity
of lead is enhanced in acidic waters, as the chemical equilibrium shifts
in the direction of free ion formation.
Often, other heavy metals are found in waters polluted with lead
from mining runoff or "atmospheric emissions. Copper, zinc, mercury, and
cadmium are toxic to varying degrees, and have some similar effects on
aquatic life. In combination, heavy metals may either have a synergistic
or antagonistic interaction with respect to .toxicity. Gray and Ventilla
(1973) combined zinc, mercury, and lead ions in solution to determine
the effect on Cristigera protozoa. The growth rate was inhibited by
67.2%, compared with the theoretical reduction of 37.4% calculated from
combining the individual effects of the metals (i.e., a synergistic
effect was observed).
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Other studies have also examined heavy metal interactions with lead.
Pietilainen (1975) indicates that cadmium increased the toxicity of lead
to phytoplankton communities if the cadmium concentration exceeded that
of lead. This effect was markedly lessened when the lead concentration
was higher. Benijts-Claus and Benijts (1975) found that both lead and
zinc had a significant adverse impact on the development of the mud
crab, Rhithropanopeus harrisi. In certain combinations, however, zinc
apparently suppressed the more toxic lead, and larval growth actually
accelerated. In toxicity tests with zebrafish, Ozoh (1979a) found that
copper and lead at the highest concentrations used (72 ug/1) were mutu-
ally suppressive with respect to growth inhibition effects.
Long-term exposure may affect the resistance of an aquatic organism.
Certain data show that fish can become acclimated to some chemicals so
that their tolerance is increased, particularly if previous generations
were exposed. Although no multi-generational studies were available for
lead, Davies et al. (1976) reported that sensitivity actually decreased
in rainbow trout when exposed as eggs; specimens exposed after hatching
were more resistant.
6.1.5 Terrestrial Organisms
6.1.5.1 Animals
Most of the information on lead toxicity to wildlife is concerned
with effects on waterfowl because of the concern for the extensive lead
poisoning as a result of the consumption of spent lead shot (see
Section 6.2). Other studies provide data on lead toxicosis in doves
and gallinaceous birds. Most of the studies on lead in wildlife, other
than waterfowl, deal primarily with tissue residues, because lead poison-
ing has seldom been observed in the field (see Section 4.2).
The symptoms generally associated with lead poisoning in waterfowl
are lethargy, anorexia, weakness, flaccid paralysis, emaciation, anemia,
greenish diarrhea, im-paction of the proventriculus, and distention of
the gallbladder (Clemens _et al.. 1975). Most toxicity tests with birds
involve feeding the birds a certain number and type (size) of shot.
Lead shot is particularly harmful to birds because the gizzard grinds
the accumulated shot into a fine powder that is easily absorbed in the
acidic conditions of the digestive tract. In mammals, on the other hand,
the shot normally passes through the digestive system, with only super-
ficial contact and absorption (Hartung 1973).
Of the numerous experiments that have been conducted to assess the
toxicity of lead in birds, a representative sample is presented below.
Further discussion is contained in Forbes and Sanderson (1978). Irby et al.
(1967) fed game farm mallards (Anas platyrgynchos) with 8, No. 6 lead shot"
each; the birds survived an average of 17 days after the dosage, and lost
an average of 37% of their initial body weight. Seven captive Canada
geese (Branta canadensis) dosed with 10 or more lead pellets died within
23 days (mean of 10 days), while two other geese fed 5 pellets survived
6-9
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Evidence illustrates that diet plays a considerable role in the
degree to which lead affects various waterfowl species. Lead pellets in
mallards on a high fiber diet lost 46% of their initial weight within
20 days after dosing, while pellets in ducks fed a low fiber diet lost
bl/, of their initial weight during the same period (Clemens et al. 1974)
Jordan and Bellrose (1951) found that the effects of dietaryleld in
mallards were most severe in birds fed a diet of whole corn. Effects
were less pronounced when the mallards were fed smaller seeds such as
wheat, rice, and millet; when a grain diet was supplemented with aquatic
greens, toxicosis was further mitigated. Holmes (1975) reported that the
addition ot egg albumen, oyster shell, calcium carbonate, and phosphorous
to mallard feed reduced the degree of lead toxicity bv 50% over a straight
corn diet. ' =
Of the waterfowl species, the mallard appears to be the most susceo-
tible to lead poisoning. Bellrose (1959) observed three species of ducks
feeding in flooded chufa beds. Mallards browsed on bottom tubers pin-
tail (Anas acuta) ate both bottom tubers and floating seeds, while green-
winged teal (A. cardinensis) limited their diet to floating seeds only
The mallards had a mortality rate ( 0.97%) ten times that of pintail/
while no lead-poisoned teal were found. The author attributed the
differential mortality rates to a higher incidence of lead in the gizzards
of bottom-feeding ducks, which mistake lead pellets for aquatic seeds or
grit Diving species, such as redhead (Ay_thya americana). ring-necked
duck (A. collaris). and canvasback (A. valisneria) are also thought to be
more susceptible to lead poisoning, although mallard mortality is usually
higher because of their preference for large seeds (Bellrose 1964).
6.1.5.2 Plants
Abundant data are available on the effects of lead on both wild and
crop plants, partly because of the concern for the human consumption of
lead. As with animals, lead has not been shown to be essential for plant
growth. Even low levels may cause growth irregularities.
In a few instances, low concentrations of lead have been found to
stimulate the growth of various crop plants, including barley, corn,
wheat, buckwheat and sugar. However, toxicosis is more often observed.
Cultivated grasses exhibit an extremely wide range of sensitivities; for
example, in one experiment, maize (Zea mays) and rye (Secale cereale)
showed no signs of toxicosis at lead acetate concentrations up to 100 mg/1.
On the other hand, barley, oats, and particularly wheat were damaged at
levels well below 100 mg/1 (Holl and Hampp 1975).
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Bean (Phaseolus vulgaris) plants were exposed to lead at concentra-
tions of 33-33,000 mg/1. At the lower limit, growth was stimulated,
while no effects were apparent at 330 mg/1. At 33,000 mg/1, the plants
were visibly damaged within 30 minutes, and died within 24 hours (Holl
and Hampp 1975). Differentiating young tissues tended to be more
sensitive to lead than mature tissues.
Other toxicity data indicate that lead affects the photosynthetic
process (Miles et a_l. 1972). Lead chloride concentrations as low as
14 mg/1 reduced chlorophyll synthesis significantly in oat seedlings;
moreover, lead levels up to 140 mg/1 inhibited chlorophyll b_ bynthesis
to a greater extent than the chlorophyll ja synthesis (Hamp and Lendzian
1974).
Airborne lead is another potential exposure pathway that may have
sublethal effects on plants. Bouganvillaea plants exposed to -7 ppm
tetraethyl lead vapor at 25°C for 3 days abscised an average of 14% of
their leaves. Total recovery was observed 14 days after the exposure
period (Siegal et al. 1973). Davis and Barnes (1973) report that 41-410
mg/1 lead chloride in watering solutions reduced the stem and root dry
weights and height of loblolly pine (Pinus taeda) and red maple (Acer
rubrum) seedlings in two forest soils. At higher concentrations, root
systems also became reduced and blackened.
Lead toxicity to plants depends on the chemical composition of the
soil. As with aquatic organisms, the presence of calcium, phosphates,
and other ions inhibit the effects of lead on plants. Acidic soils
increase plant susceptibility to lead, as does increased soil temperature.
The levels of organic nutrients and soluble silicon may also affect lead
uptake in and availability to plants (NSF 1977).
6.1.6 Summary
Lead may cause acute toxicosis to aquatic organisms at concentrations
as low as 0.3 mg/1. Sublethal effects have been observed in rainbow trout
in lead concentrations of 7.6 yg/1. It appears as if freshwater inver-
tebrates have a narrower range of lead sensitivities than fish, although
this result could be a function of the test species chosen. Aquatic micro-
flora have exhibited toxic effects in lead levels between 0.05 mg/1 and
28.0 mg/1. The mummichog was the only marine finfish tested for acute
toxicosis; the reported 96-hour LC$Q was 315 mg/1. Marine invertebrates
exhibited toxicosis (acute, chronic, and sublethal) in lead concentra-
tions between 0.05 mg/1 and >500 mg/1.
Several water parameters strongly influence the aquatic toxicity of
lead. When the water hardness was raised from 28-353 mg/1, the 96-hour
LC50 for rainbow trout increased by a factor of >400. Similar toxicity-
suppressing effects of water hardness were observed for fathead minnow
and bluegill. The presence of phosphates, chelating agents, and nutrients
has also been observed to reduce lead toxicity. Water with a low pH
shifts the equilibrium of aqueous lead toward free ion formation, which
increases toxicity. Heavy metal interactions with lead may be either
6-11
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synergistic or inhibitory, depending on the specific combination. Rela-
tively little information exists on the comparative toxicity of various
rorms of lead.
With the consideration of all of these variables, a range of lead
concentrations can be categorized for toxicity as shown below. These
ranges are only a very general guide for the assessment of the potential
ecological impact of a given lead concentration in an aquatic environment,
• 10 ug/1 Life-cycle toxicity test in soft water produced
abnormal development in rainbow trout. All
other species tested are unaffected.
• 10-100 ug/1 Sublethal effects, such as tail and fin
degeneration, reported for several freshwater
fish species in soft water, as well as growth
inhibition in sensitive freshwater algae.
Chronic toxicity reported in soft water and
are based on the effects on early life stages
in fish and life cycle test in Daphnia.
• 100-1000 Sublethal toxicosis in a variety of freshwater
"S/1 fish and invertebrates in soft and moderately
hard water. Acute effects observed in
stickleback and some invertebrates. Numerous
species of freshwater algae adversely affected,
as well as more sensitive marine microflora.
• 1.0-10.0 Acute toxicity level for several freshwater
m8/! fish and invertebrate species in soft water
and for sensitive marine invertebrates.
Algicidal for some marine algae.
• 10.0-100 Acute effects observed in a variety of fresh-
mS/l water fish and in most invertebrates tested.
All algae species tested sensitive in this
range.
• 100 mg/1 Only the most resistant species (e.g. red
shiner, mosquitofish, cockle) are able to
survive, even for short periods, in this
range of concentrations. Tolerance to such
levels would be increased in hard water.
To protect freshwater aquatic life, the U.S. EPA (1980) has estab-
lished a function of the criterion for lead (as total recoverable lead)
hardness, i.e., e (2.35 [In hardness]-9.48) as a 24-hour average, and
the concentration (in pg/1) should not exceed e C1-22 Un hardness]-0.47)
At hardness of 50, 100, and 200 mg/1 as CaC03, the criteria are 0.75, 3.8*,
and 28 ug/1, respectively as a 24-hour average and the respective maxima
would be 74, 170, and 140 ug/1.
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Data on lead toxicity in waterfowl, doves, and gallinaceous birds
are plentiful, and indicate that the ingestion of spent lead shot can
be lethal. Mallards and diving ducks are particularly susceptible,
largely as a result of feeding habits rather than physiological vulner-
ability.
Lead toxicosis has been observed in terrestrial plants from lead
concentrations ranging from 0.005-33,000 mg/1 in culture or watering
solutions. Effects include growth stimulation (at very low levels),
growth inhibition, leaf yellox^ing, abscission, inhibition of mitosis
and chlorophyll synthesis, loss of turgor pressure, and death. Lead
toxicity to plants is mitigated by factors similar to those in aquatic
environments, i.e., high pH, high calcium and phosphate levels; in
addition, the temperature, organic nutrient and soluble silicon content
of the soil influence the toxicity of lead.
6.2 EXPOSURE TO BIOTA
6.2.1 Introduction
Lead is a pervasive element that appears at various concentrations
in air, water, and soil systems, as well as in the tissues of organisms
(see Section 4.2). In this section, lead exposure levels to aquatic
and terrestrial biota are discussed, with special focus on factors that
lead to acute and chronic exposure. For aquatic life, the following
topics are reviewed:
• The various pathways of exposure in fish, invertebrates,
and algae;
• Chemical parameters in the aquatic environment that may
affect the degree of exposure to lead and uptake of the
metal by biota;
• Areas of the country in which relatively high lead concen-
trations were reported in 1979; and
• Recent incidents of elevated lead exposure in various
water bodies.
Data on lead exposure to terrestrial mammals are limited mainly to
comparative residue studies on rodents in urban and rural locations. A
considerable amount of information on lead in waterfowl is available,
as a result of the widespread problem of exposure to spent lead shot.
Habitat conditions and other factors, such as hunting pressure, are
described for their effects on the availability of lead 'shot for inges-
tion by waterfowl.
Terrestrial plants are exposed to elevated lead concentrations
primarily in the vicinity of anthropogenic sources. The chemical
properties of the soil are crucial in determining the availability of
lead.
6-13
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6.2.2 Aquatic Organisms
6.2.2.1 Pathways of Exposure
The three general pathways of exposure in aquatic fauna consisting
of diet, direct absorption from the water, and contact (dermal or
dietary) with sediment. As with other heavy metals, relatively few
studies attempt to evaluate the relevance of each of these pathways to
different species. Moreover, the available data provide conflicting
evidence concerning routes of uptake, particularly with fish.
Lead residues in many invertebrates reflect levels found in sedi-
ment; however, it remains unclear whether the lead is strongly concen-
trated from water or absorbed from sediment. Tubificid worms collected
by Mathis and Cummings (1973) reported lead residues equivalent to
sediment concentrations, while aqueous lead levels were four orders of
magnitude lower.
McNurney and co-workers (1977) measured residues in a variety of
freshwater stream organisms and found a positive correlation between
lead burden and the degree of sediment contact. Burrowing oligochaetes
and insect larvae had the highest lead residues, followed by fauna
(pelecypods, crayfish, darters) subsisting at the sediment-water inter-
face. Lower residues were detected in bottom-feeding omnivorous fish,
while carnivores, which have very little contact with settled or sus-
pended sediments, had the lowest body burdens. The authors hypothesized
that food was the main source of lead in carnivores; however, they were
uncertain of the dominant exposure pathway for the lower organisms.
Some circumstantial evidence demonstrates that suspended sediments
and food particles are the primary source of lead to filter-feeders.
Bryan (1973) attributed seasonal changes in lead tissue levels in two
scallop species to variations in food supply in the form of suspended
matters. Bryan and Uysal (1978) concluded that the ingestion of sus-
pended sediments was the main pathway for lead uptake in the clam
(Scrobicularia plana), because lead accumulated primarily in the diges-
tive gland.
The relative importance of sediment and waterborne lead has also
been examined for fish. In long-term tests with rainbow trout (Salmo
gairdneri), Hodson £t al. (1978) added lead in various concentrations
to the diet. With doses up to 950 yg/day, the fish excreted virtually
all ingested lead. At doses between 1935 yg/day and 3160 yg/day,
approximately 50% was excreted; however, because no bioaccumulation
was observed, the authors assumed some experimental error in the analy-
sis of excreta at higher doses.
Such highly efficient depuration, at least at low concentrations,
could explain why.the predatory fish collected by NcNurney _e_t ad. (1977)
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had low lead residues despite the high body burdens in lower-order
fauna. On the other hand, Hardisty et al. (1974) discerned a distinct
correlation between tissue concentrations and crustacean consumption in
seven teleost species. Schell and Barnes (1974) found that lead resi-
dues in the northern squawfish (Ptychocheilus oregonensis) decreased
with age. One explanation was that younger fish ate zooplankton, which
are high in lead, while older fish preyed on various fish species with
low lead burdens. Butterworth _et_ al. (1972) reported a steady increase
in lead residues with ascending trophic levels in an estuary. However,
most of the evidence does not indicate significant biomagnification of
lead in food chains (Wong _et al. 1978).
In contrast to their work with exposure via ingestion, Hodson and
co-workers (1978) measured tissue concentrations in rainbow trout after
various periods of exposure to lead and found a linear relationship to
aqueous lead concentrations. High aqueous lead levels resulted in
elevated residues in the gills and kidneys, which, in turn, reflected
the direct contact of gills with lead-contaminated water and the possible
excretion of lead via urine. Thus, it is apparent that both ingestion
of lead in food sources, as well as gill contact with water can result
in exposure to lead.
6.2.2.2 Environmental Factors Affecting Lead Exposure and Uptake
«
The variables that alter the toxicity of lead to aquatic organisms
may influence the availability of lead for uptake. Acidic water shifts
the equilibrium of soluble lead toward the more toxic free ion form.
Pumpkinseed sunfish (Lepomis gibbosus) exposed to fc03Pb at pH 6.0 accumu-
lated three times as much lead as they did at pH 7.5 (Merlini and Pozzi
1977). These results suggest that free ionic lead is the form most
available for uptake.
Water hardness levels also affect the solubility of lead, and hence
its availability for absorption. Varanasi and Markey (1977) studied lead
accumulation by rainbow trout in waters of varying hardness. Calcium
(as CaCOs) had a significant mitigative effect on lead uptake rates;
however, the authors hypothesized that lead might, in turn, inhibit cal-
cium absorption required for bone growth by the trout.
The presence of other metals may affect lead uptake. Luoma and
Bryan (1978) indicated a possible antagonistic relationship between lead
and iron. Lead residues in the clam (Scrobicularia plana) were inversely
proportional to sediment concentrations of amorphic iron in 17 estuarine
locations. The strong negative correlation between these two variables
led the authors to speculate that the Pb:Fe ratio in sediments may be a
good indicator of biologically available lead.
Brown (1977) studied lead uptake bioaccumulation experiments on
three groups of isopods (Asellus meridianus) collected from different
areas. The most tolerant group accumulated the most lead, and thus
probably had a greater ability to store and detoxify the metal. The
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tolerant group also had much higher levels of sulfur, which suggests
that the detoxification mechanism was a possible sulfhydryl binding of
lead. Thus, as with toxicity, various factors appear "to affect lead
uptake and hence exposure. Such factors include pH, water hardness,
inhibition by other metals, and acclimation.
6.2.2.3 Monitoring Pat .a
The most complete data base for measured levels of ambient aqueous
lead in the U.S. river basins was found in STORET. Major basin data are
analyzed in Section 4.2. Table 6-5 lists minor basins with mean total
lead levels >50 ug/1, which represents a level at which sublethal effects
have been observed, although some chronic values of <50 ug/1 have been
reported. Lead levels of -100 ug/1 may be lethal to some species,
depending on the duration of exposure and various chemical factors.
These values are means of positive values only; thus, they reflect a
somewhat higher mean than if all the values had been included. Of the
basins listed, those with water hardness usually <50 mg/1 as CaC03 are
also identified, because soft water effectively increases lead exposure
levels.
Two minor basins had mean lead levels >100 ug/1. The Catawba-
Wateref Basin in the Southeast had an average lead concentration of
124.5 ug/1, with 50.0% of the positive observations >100 ug/1. The
Kanawha River in the Ohio River Valley had a mean lead level of
148.7 Ug/1, with 7.5% of the measurements >100 ug/1. In this case,
the mean was most likely skewed by a few extremely high measurements,
including a maximum of 7000 ug/1. Other minor basins with a relatively
high proportion of boservations (>20%) >100 ug/1 were the James River in
the North Atlantic, the Fox River-Wolf Creek drainage area near Lake
Michigan and the Kootenai River in the Northwest.
Reports in the literature of elevated lead concentrations that
result from a specific source are uncommon; thus, little opportunity is
provided to assess the effects of acute exposure in the field. Two
reports of fish kills related to lead concentrations were found. In
one, in 1970, the total lead concentration was about 1000 ug/1 at some
type of industrial operation in Glover, Missouri. The other occurred at
an old smelter site in Henrietta, Oklahoma in 1973. The reported lead
concentration was 23,600 ug/1 (U.S. EPA 1979).
6.2.3 Terrestrial Organisms
6.2.3.1 Mammals
Little information is available on lead exposure levels to mammals
probably because of the lack of observations of lead poisoning in field
situations. Most of the available studies are primarily concerned with
correlations between proximity to anthropogenic sources of lead and
residues in wild specimens.
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TABLE 6-5.
MEASUREMENTS OF TOTAL LEAD CONCENTRATIONS IN U.S. MINOR RIVER BASINS, 1979
River Basin
Ma.1 or /Minor Name
i
^i
1/33
1/34
2/3
2/16
3/7
3/9
3/13
3/24
3/28
5/3
5/7
5/9
8/24
8/25
9/8
9/12
10/8
11/4
H/5
12/4
13/1
13/3
15/7
Lower Hudson — NY Metropolitan Area
New Jersey Coast
Delaware River — Zone 1
James River
Yadkin-Pee Dee-Lower Pee Dee River
Catawba-Wateref, Congaree, Santee-Cooper Res.
Edisto-Combahef River
Savannah River
Tampa Bay Area
Lower Florida Area
Beaber River
Kanawha River
Big Sandy River
Green Bay Western Shore
Fox River — Wolf Creek
Lower Platte River from North Platte
Lower Missouri River from Niobrara River
North Canadian River
Lower Colorado River
Middle Colorado River — San Juan River
Gila River
Green River
Brazos River
Kootenai River
Spokane River
Santa Ana River
Northwestern Lahontan
Great Salt Lake
Mean
>5°
Basins with >. 10 measurements in 1979.
b!978 data.
Note: There are 307 minor river basins in the continental U.S.
Source: U.S. EPA C1980).
*
*
*
*
*
*
*
*
A
*
~10% of Pb *50* of Hardness
>100 iig/1 Measurements <50
*
*
*
*
*
*
*
*
*
-------
Williamson and Evans (1972) examined the lead burdens in a variety
of small mammals, and found no evidence of biomagnification in food
chains. Though carnivorous shrews generally had higher residues than
herbivorous mice, both groups contained less lead than their respective
food sources. Shrews and mice collected close to roads had higher lead
burdens than specimens collected at distances from roads.
In a study of lead residues in voles and field mice in England,
Jeffries and French (1972) found similar results. Body burdens ranged
from an average of 4.19 yg/g dry weight on woodland and arable sites
to 5.98 jjg/g near minor roads to a maximum of 7.00 ug/g near a busy
highway. Mouw et al. (1975) found that lead residues in the bones" and
kidneys of urban rats were twenty times greater than those in rural rats,
while concentrations in feces were four times higher. Rolfe and Haney
(1975) analyzed eight species of small mammals in Illinois to determine
the effects of proximity to roadways. Except for two species, animals
trapped along medium-use roads had tissue levels intermediate to those
captured along high- and low-use roads. These authors detected no
seasonal variations in tissue concentrations of lead. Thus, evidence
of elevated exposure to lead in terrestrial mammals has been observed
in the vicinity of highways.
6.2.3.2 Birds
There are several possible pathways for lead exposure to birds.
Bagley and Locke (1967) indicate that all birds are regularly exposed to
sublethal levels of lead in their food. Atmospheric lead fallout
(originating from industrial and auto emissions) is a potential exposure
route; however, more data must be acquired on this potential exposure
route. Still, Forbes and Sanderson (1978) have recorded several reports
of waterfowl mortality caused by runoff from mine wastes and ingestion
of mine tailings.
One source, however, appears to account for nearly all cases of
lead toxicosis in birds. Each year, over 3000 tons of lead shot are
deposited by waterfowl hunters in marshes, lakes, and fields of the
United States, while as many as 122,000 lead pellets per acre have been
found in some areas (U.S. FWS 1976). Numerous species ingest the spent
shot, mistaking it for grit or plant seeds, or eating it by accident as
they forage.
Many instances of lead-related waterfowl kills in large numbers
have been reported; written accounts date from as early as 1894 (Grinnell
1894). Quortroup and Shillinger (1941) concluded that lead poisoning
was the third most important (8.6% of the total) cause of death in 3000
specimens taken from various western lakes. Perhaps, because of the
increased monitoring of waterfowl populations, such incidents have been
reported more frequently over the last 30 years. In the most comprehen-
sive survey, Bellrose (1959) reported 34 waterfowl die-offs in the United
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States, between 1937 and 1957, with mortalities ranging from 100 to
16,000 in each event. Die-offs occurred in each of the four major
flyways (Atlantic, Mississippi, Central, and Pacific); the greatest
number of casualties occurred in the Mississippi flyway. However,
Jordan and Bellrose (1951) believe that small, day-to-day losses
constitute a larger portion of total lead-related mortalities than
spectacular die-offs that receive more publicity.
Many factors may influence lead exposure levels to waterfowl.
First, the hunting pressure determines how much lead shot will be
scattered over a given area. As a measure of hunting pressure, the
U.S. FWS (1976) estimated waterfowl hunter days in each of the major
flyways for the period 1952-71. The Mississippi flyway had 40-45% of
the total hunter days, the Central flyway had >20%, and the Atlantic
and Pacific flyways each had <20% of the hunting activity.
The characteristics of lake and marsh bottoms also affect exposure
levels; for example, in soft lake beds the lead shot sinks into sedi-
ment, which renders it relatively unavailable for consumption. Bellrose
(1959) found that in such areas, little of the exposed shot is carried
over from one year to the next; therefore, more lead shot would probably
be available during and soon after the hunting season. On hard bottoms,
however, spent shot may simply accumulate on a yearly basis. The ice
cover and prevailing water levels also affect the degree of exposure,
because they determine the size of the area in which waterfowl may come
into contact with spent shot (Forbes and Sanderson 1978).
Dietary factors are important in lead exposure to waterfowl. Birds
that consume mostly large quantities of corn are generally more suscep-
tible to lead poisoning (Bellrose 1964). Various toxicity studies (see
Section 6.1.5.1) have shown that diets high in calcium, phosphorous,
and other nutrients led to decreased sensitivity in ducks. The addition
of smaller grain seeds and aquatic plants to the diet mitigate the toxic
effects of lead to some degree (Jordan and Bellrose 1951). Moreover,
birds consuming large quantities of food are apparently less likely to
experience lead poisoning (Bellrose 1964).
Because the various waterfowl have different feeding habits, some
species naturally have greater levels of exposure. Diving ducks, on the
whole, are more likely to ingest lead pellets because they feed on seeds,
tubers, and rootstocks at lake bottoms. Lead pellets may be mistaken
for certain aquatic seeds because of their similar size and shape; thus,
they are consumed. Bellrose (1959) examined the gizzard contents of
waterfowl bagged by hunters; he found the highest incidence of lead shot
in diving ducks. Between 12 and 14% of all canvasback, redhead, lesser
scaup, and ring-necked ducks had ingested lead pellets that had remained
in the gizzard. In addition, birds that prefer corn, such as Canada
geese, mallards, pintail and other species of dabbling ducks, ingest more
lead pellets than most other types of waterfowl.
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Lead poisoning has been reported in other types of birds; however,
it is, in general, a rare phenomenon. Calvert (1876) and Holland (1882)
reported pheasants ill from ingesting lead shot. Of 1977 gizzards of
Gruiformes (cranes and rails), only 49 had lead shot, and nearly one-half
were from sora rails. Jones (1939) doubted that cranes or limpkins ever
ingested spent shot. Campbell (1950) reported the finding of a dead
scaled quail with 13 lead pellets in its crop. In 1949 gizzards from
doves taken by hunters, Lewis and Legler (1968) found a 1% incidence of
lead pellets. A University of Minnesota study cited by the U.S. FWS
(1980) found that one-fourth of the castings beneath bald eagle roosting
trees contained lead shot. Several deaths from lead poisoning in bald
eagles have been reported; mortality is more likely if the shot is
retained in the digestive tract rather than cast (U.S. FWS 1980).
Lead accumulates in various bird tissues, most notably in bones.
According to the U.S. FWS (1976), low-level chronic exposure to lead
(as in diet) results in comparatively high levels in bones, lower levels
in liver and kidney, and still lower levels in heart, lung, muscle, and
brain. High levels in liver and kidney as well as bone are indicative
of recent acute exposure. One experiment cited by the U.S. FWS (1976)
demonstrated that the ingestion of a single lead pellet can produce high
lead concentrations in the wing bones of ducks. Of the 28 species of
birds examined by Bagley and Locke (1967), tissues from the osprey, an
aquatic predator, had the highest lead burdens.
Several studies have been conducted to determine the effect of
urban versus rural environments on lead residues in birds. Tansy and
Roth (1970) found that pigeons in urban areas had higher lead residues
in bone, feathers, and kidneys than their rural counterparts, although
concentrations in blood were similar. Ohi _et al. (1974) also compared
rural with urban pigeons; they found the greatest differences in the
femur (bone), ALA-D enzyme activity, and blood. Getz et_ al. (1977)
measured lead residues in five passerine (songbird) species", and found
that urban specimens had uniformly higher burdens in feathers, butt, liver,
lung, kidney, bone, and muscle.
6.2.3.3 Terrestrial Plants
The potential for exposure of terrestrial flora to lead increases in
areas of high lead particulate deposition. Sources contributing high levels
to the atmosphere include lead smelters, highways, various stack-discharging
industries, and urban areas in general. Mining areas have high associated
levels of lead in soil. Section 4.2 (Tables 4-4 to 4-6) presents concentra-
tions in air, soil, and vegetation associated with specific sources. Lead
may be absorbed from deposition directly on leaves and stems or taken up
from soil contaminated by particulate fall-out. Higher exposure levels
are associated with direct deposition; however, cuticle barriers and
washing off during rain or wind activities reduce the concentrations
taken up by plants (see Section 4.3). Soil-originated exposure levels
are usually lower but more persistent as a result of immobilization of
lead in the upper soil profile. Once lead is taken up into vegetation,
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it is likely to persist, and will recycle into the system with the carbon
cycle.
Environmental factors influencing plant uptake of lead from soil
and subsequent exposure include pH, presence of other nutrients and metals,
and species acclimation. Low soil pH is favorable to uptake (MacLean et al.
1969); thus, standard agricultural practices (e.g. liming of soil) may
decrease accumulation. The presence of calcium ions inhibits lead uptake
(Wilkins 1957), and phosphate deficient plants are more susceptible to lead
effects than normal plants (Koeppe and Miller 1970). In addition, Peterson
(1978) has observed lead-tolerant ecotypes for several floral species that
have had long-term exposure to the metal.
6.2.3.4 Summary
There are several possible pathways of lead exposure to aquatic
fauna, including water, diet, and sediment. Most likely, contact with
sediment is an important exposure route, particularly for benthic inver-
tebrates and filter feeders. However, the assertion that sediment is the
most important pathway for these organisms is based largely on circumstan-
tial evidence; such conclusions must be verified by experiments that
isolate the effects of water-borne and sediment-borne lead. Data on lead
uptake by fish are scarce, although there is evidence for uptake from
water and diet. However, sediment remains a potential direct or indirect
source of large quantities of lead for invertebrates and vertebrates alike.
Lead exposure to aquatic organisms is enhanced by soft, acidic
waters, and the presence of lead sources, such as industrial or automo-
tive emissions, lead mines, and urban areas in general.
For minor river basins, STORET monitoring data indicate that mean
total lead concentrations were generally <50 yg/1 in 1979. Furthermore,
because biologically available lead comprises only a fraction of total
lead, exposure levels are normally well below 50 yg/1. Minor basins
with relatively high concentrations are listed in Table 6-5. Only a few
instances of fish kills caused by lead have been reported; however,
elevated residues have been observed in areas with high aqueous lead
levels.
Information on mammals is limited mainly to studies of rodents
with varying degrees of exposure to urban and automotive lead. One
study reported no evidence of lead biomagnification from food sources
for shrews and mice.
Over the last century, there have been numerous reports of water-
fowl mortality as a result of the ingestion of spent lead shot. Water-
fowl kills are more prevalent in areas under heavy hunting pressure (such
as the Mississippi flyway) and in lakes and marshes with hard bottoms,
where lead shot can accumulate. Exposure is also greater for diving
ducks, which have access to lead on lake bottoms, and for species that
eat mainly large seeds, such as corn. Lead poisoning is relatively rare
6-21
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in other types of birds. However, species dwelling in urban areas (e.g.,
pigeons) are reported to have higher lead residues than their rural coun-
terparts. Lead accumulates most strongly in the bones of all species
examined.
Lead exposure to terrestrial plants increases above background
levels in areas of high lead particulate deposition. As for other
organisms, sources include lead smelters, automobiles, various indus-
tries, and urban areas in general. Lead may be absorbed either through
leaf or root tissues; direct deposition on leaves comprises a larger
proportion of lead exposure than lead in soil; however, cuticle barriers
and washing off will reduce absorption through leaves. Soils with low
pH and calcium content are conducive to uptake through the roots. In
natural conditions, lead poisoning is extremely rare; however, elevated
residues in crop plants may increase human exposure levels.
The significance of high, but non-toxic, levels of lead in plants
in this exposure assessment should be stressed. Human exposure through
the ingestion of contaminated crops by humans can be an important path-
way, which is described in Section 5.2. Non-human biota ingesting
vegetation may be similarly exposed.
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REFERENCES
Anderson, R.V. The effects of lead on oxygen uptake in the crayfish,
Oronectes virilis (HAGEN). Bull. Environ. Contam. Toxicol. 20:394-400;
1973.
Bagley, G.E.; Locke, L.N. Bull. Environ. Contam. Toxicol. 2:297-305;
1967. (As cited by Forbes and Sanderson 1978)
Barber, R.T.; Ryther, J.H. J. Exp. Mar. Biol. Ecol. 3:191-199; 1969.
(As cited by Wong _et al. 1978)
Battelle Columbus Laboratories (BCL). Water quality criteria data book.
Volume 3: Effects of chemicals on aquatic life. Contract No. 68-01-0007.
Washington, DC: U.S. Environmental Protection Agency; 1971.
Bell, M.A.; Ewing, R.A.; Lutz, G.A.; Holoman, V.L.; Paris, B.; Krause, H.H.
Reviews of the environmental effects of pollutants: VII. Lead. Report
No. EPA-600/1-78-029. Washington, DC: U.S. Environmental Protection
Agency; 1979.
Bellrose, F.C. 111. Nat. Hist. Surv. Bull. 27:235-288; 1959. (As cited
by Forbes and Sanderson 1978)
Bellrose, F.C. Waterfowl tomorrow. Washington, DC: U.S. Fish and Wild-
life Service; 1964: 479-485. (As cited by Forbes and Sanderson 1978)
Benijts-Claus, C.; Benijts, F. In: Koeman, J.H.; Strik, J.J. eds.
Sublethal effects of toxic chemicals on aquatic animals. Amsterdam:
Elsevier; 1975. (As cited by U.S. EPA 1978)
Biesinger, K.E.; Christensen, G.M. The effect of various metals on
survival, growth, reproduction and metabolism of Daphnia magna. J. Fish.
Res. Bd. Can. 29:1691-1700; 1972. (As cited by Wong et al. 1978)
Brown, B.E. Observations on the tolerance of the isopod Asellus meridianus
Rac. Freshwater Biol. 7:235-244; 1977. (As cited by Phillips and Russo 1978)
Brown, B.E. Uptake of copper and lead by a metal-tolerant isopod
Asellus meridianus Rac. Freshwater Biol. 7:235-244;. 1977. (As cited
by Phillips and Russo 1978)
Brown, B.; Ahnsulla, M. Mar. Pollut. Bull. 2:182; 1971. (As cited by
Tornabene gt_ al. 1977)
Bryan, G.W. J. Mar. Biol. Assn. (U.K.) 53:145-166; 1973. (As cited by
Wong et al. 1978)
Bryan, G.W.; Uysal, H. Heavy metals in the burrowing bivalve
Scrobicularia plana from the Tamar estuary in relation to environ-
mental levels. J. Mar. Biol. Assn. (U.K.) 58:89; 1978. (As cited
by Leland ejt al. 1979)
6-23
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Butterworth, J.; Lester, P.; Nickless, G. Mar. Pollut. Bull. 3-72-74-
1972. (As cited by Wong et al. 1978) '
Calvert, H.S. The Field 47:189; 1876. (As cited by Forbes and Sanderson
Campbell, H. J. Wildlife Managmt. 14:243-244; 1950. (As ciced by Forbes
and Sanderson 1978)
Christensen, G.M. Biochemical effects of methylmercuric chloride
cadmium chloride and lead nitrate on embryos and alevins of the brook
trout. Toxicol. Appl. Pharmacol. 32:191-197; 1975. (As cited by
Wong _et al. 1978)
Clemens, E.T.; Krook, L.; Aronson, A.L.; Stevens, C.E. Pathogenesis of
lead shot poisoning in the mallard duck. Ithaca, NY: Cornell University
Depts. Physiol., Biochem., Pharmacol., and Pathol., N.Y. State Vet.
College; 1974. 28 p. (As cited by Forbes and Sanderson 1978)
Clemens, E.T.; Krook, L.; Aronson, A.L.; Stevens, C.E. Pathogenic
lead shot poisoning in the mallard duck. Ithaca, NY: Cornell University,
N.Y. State Vet. College; 1975: 248-285. (As cited by U.S. EPA 1977)
Cook, R.S.; Trainer, D.O. J. Wildlife Managmt. 30:1-8; 1966. (As cited
by Forbes and Sanderson 1978)
Damron, B.L. ; Wilson, H.R. Bull. Environ. Contain. Toxicol. 14:489-496;
1975. (As cited by Forbes and Sanderson 1978)
Davies, P.H.; Goettl, J.P. Jr.; Sinley, J.R.; Smith, N.F. Acute and
chronic toxicity of lead to rainbow trout Salmo gairdneri in hard and
soft water. Water Res. 10:199-206; 1976.
Davis, J.B.; Barnes, R.L. Effects of soil-applied fluoride and lead
on growth of loblolly pine and red maple. Environ. Pollut. 5(l):35-44-
1973. (As cited by Bell et al. 1979)
Billing, W.J.; Healey, C.W.; Smith, W.C. Ann. Appl. Biol. 13sl68-176;
1926. (As cited by Wong et al. 1978)
Diters, R.W.; Nielsen, S.W. Lead poisoning of raccoons in Connecticut.
J. Wildlife Dis. 14:187-191; 1978.
Doelman, P. Lead and terrestrial microbiota. Nriagu, J.O. ed. The
biogeochemistry of lead. New York, NY: Elsevier-North Holland Biomedical
Press; 1978.
Dorfman, D. Tolerance of Fundulus heteroclitus to different metals in
salt waters. Bull. New Jersey Acad. Sci. 22(2):21-23; 1977.
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Drucker, H.; Wildung, R.E. eds. Biological implications of metals in
the environment. Proceedings of the fifteenth annual Hanford life
sciences symposium; 1975 September 29-October 1. Richland, WA; 1977.
Available from: Technical Information Center, USERDA.
Forbes, R.M.; Sanderson, G.C. Lead toxicity in domestic animals and
wildlife. Nriagu, J.O. ed. The biogeochemistry of lead in the
environment. New York, NY: Elsevier-North Holland Biomedical Press;
1978.
Gale, N.L.; Hardie, M.G.; Jennett, J.C.; Aleti, A. Transport of trace
pollutants in lead mining wastewaters. Hemphill, D.D. ed. Trace sub-
stances in environmental health-VI. Proceedings of the University of
Missouri 6th annual conference on trace substances in environmental
health; 1970 June 23-25, Columbia, MO: University of Missouri; 1973.
(As cited by Bell et al. 1979)
Getz, L.L.; Best, L.B.; Prather, M. Lead in urban and rural song birds,
Environ. Poll. 12:235-238; 1977. (As cited by U.S. EPA 1977)
Gray, J.S.; Ventilla, R.J. Ambio 2:118-121; 1973. (As cited by
Wong et al. 1978)
Grinnell, G.B. Lead poisoning. Forest and Stream 42(6):117-118; 1894.
(As cited by U.S. FWS 1976)
Hampp, R.; Lendzian, K. Effect of lead ions on chlorophyll synthesis.
Naturwiss. 61(5) :218-219; 1974. (As cited by Bell e_t al. 1979)
Hannan, P.J.; Patouillet, C. In: Ruivo, M. ed. Marine pollution and
sea life. London, England: Fishing News Ltd.; 1978. (As cited by
Wong et al. 1978)
Hardisty, M.W.; Kartar, S.; Sainsbury, M. Mar. Pollut. Bull. 5:61-63;
1974. (As cited by Wong et al. 1978)
Hartung, R. Biological effects of heavy metal pollutants in water.
Adv. Exptl. Med. Biol. 40:161-172; 1973.
Hodson, P.V.; Blunt, B.R.; Spry, D.J. Chronic toxicity of water-borne
and dietary lead to rainbow trout (Salmo gairdneri) in Lake Ontario
water. Water Res. 12:869-878; 1978.
Roll, W.; Hampp, R. Lead and plants. Residue Rev. 54:79-111; 1975.
(As cited by Bell et al. 1979)
Holland, G. The Field 59:232; 1882. (As cited by Forbes and Sanderson
1978)
Holmes, R.S. Lead poisoning in waterfowl — dosage and dietary study.
111. Nat. Hist. Surv., Olin Corp., Winchester Group; 1975: 70 p.
(As cited by Forbes and Sanderson 1978)
6-25
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Irby, H.D.; Locke, L.N. ; Bagley, G.E. J. Wildlife Managmt. 31:253-257;
1967. (As cited by Forbes and Sanderson 1978)
Jeffries, D.J.; French, M.C. Lead concentrations in small mammals
trapped on roadside verges and field sites. Environ. Poll. 3:147-156-
1972. (As cited by U.S. EPA 1977)
Jones, J.R.E. The relative toxicity of salts and lead, zinc., and copper
to the stickleback (Gasterosteus aculeatus L.) and the effect of calcium
on the toxicity of lead and zinc salts. J. Exp. Biol. 15:394-407; 1938.
(As cited by Battelle Columbus Laboratories 1971)
Jones, J.C. J. Wildlife Managmt. 3:353-357; 1938. (As cited by Forbes
and Sanderson 1978)
Jones, L.H.; Clement, C.R.; Hopper, M.J. Lead uptake from solution by
perennial ryegrass and its transport from roots to shots. Plant Soil'
38(2):403-414; 1973. (As cited by Bell et al. 1979)
Jones, M.B. Synergistic effects of salinity, temperature, and heavy '
metal on mortality and osmoregulation in marine and estuarine isopods
(Crustacea). Mar. Biol. 30:13-20; 1975.
Jordan, J.S.; Bellrose, F.C. Lead poisoning in wild waterfowl. 111.
Nat. Hist. Biol. Notes 26:1-27; 1951. (As cited by U.S. FWS 1976)
Kaplan, H.M. .et al. Toxicity of lead nitrate solutions for frogs (Rana
pipiens). Lab. Anim. Care 17:240; 1967. (As cited by U.S. EPA 1978d)
Kemp, H.T.; Little, R.L.; Holoman, V.L.; Darby, R.L. Water quality
criteria data book - Vol. 5. Effects of chemicals on aquatic life.
Washington, DC: U.S. Environmental Protection Agency; 1973.
Koeppe, D.E.; Miller, R.J. Lead effects on corn mitochondrial respira-
tion. Science 167:1376-1377; 1970. (As cited by Bell et_ al. 1979)
Leland, H.V. et_ al. Bioaccumulation and toxicity of heavy metals and
related trace elements. J. Water Poll. Control Fed. 51(6):1592-1616;
1979.
Lewis, J.C.; Legler, E. J. Wildlife Managmt. 32:476-482; 1968. (As
cited by Forbes and Sanderson 1978)
Lloyd, R. J. Exp. Biol. 38:447-455; 1961. (As cited by Wong jet al. 1978)
Luoma, S.N.; Bryan, G.W. Factors controlling the availability of sedi-
ment-bound lead to an estuarine bivalve. J. Mar. Biol. Assn. (U.K.)
58:793; 1978. (As cited by Leland et al. 1979)
MacLean, A.J.; Halstead, R.L.; Flinn, B.J. Extractability of added lead
in soils and its concentration in plants. Can. J. Soil Sci. 49(3):
327-335; 1969. (As cited by Bell et al. 1979)
6-26
-------
MacPhee, C.; Ruelle, R. Lethal effects of 1888 chemicals upon four
species of fish from western North America. University of Idaho, Forest,
Wildlife, and Range Expt. Stn. Bull. No. 8; 1969. (As cited by Wong
et_al. 1978)
Mathis, B.J.; Cummings, T.F. Selected metals in sediments, water, and
biota, in the Illinois River. J. Water Poll. Control Fed. 45(7):1573-
1583; 1973.
Matthiesson, P.; Brafield, A.E. Uptake and loss of dissolved zinc by
the stickleback Gasterosteus aculeatus L. J. Fish Biol. 10:399; 1977.
McNurney, J.M.; Larimore, R.W.; Wetzel, M.J. Distribution of lead in
the sediments and fauna of a small midwestern stream. Drucker, H.;
Wildung, R.E. eds. Biological implications of metals in the environment.
Proceedings of the fifteenth annual Hanford life sciences symposium;
1975 September 29-October 1, Richland, WA; 1977. Available from:
Technical Information Center, USERDA.
Merlini, M.; Pozzi, G. Lead and freshwater fishes: Part 1 — lead
accumulation and water pH. Environ. Pollut. 12:168-172; 1977. (As
cited by Phillips and Russo 1978)
Miles, C.D.; Brandle, J.R.; Daniel, D.J.; Chu-Der, 0.; Schnare, P.O.;
Uhlik, D.J. Inhibition of photosystem II in isolated chloroplasts by
lead. Plant Physiol. 49(5):820-825; 1972. (As cited by Bell ot al. 1979)
Miller, J.C.; Landesman, R. Reduction of heavy metal toxicity to Xenopus
embryos by magnesium ions. Bull. Environ. Contain. Toxicol. 20:93-95; 1978.
Morgan, G.W.; Edens, F.W.; Thaxton, P.; Parkhurst, C.R. Poult. Sci.
54:1636-1642; 1975. (As cited by Forbes and Sanderson 1978)
Mouw, D.; Kalitas, K.; Anvev, M.; Schwartz, J.] Constan, A.; Hartung, R.;
Cohen, B.; Ringler, D. Lead. Possible toxicity in urban vs. rural rats.
Arch. Environ. Health 30(b):276-280; 1975. (As cited by Bell ^t al. 1979)
National Science Foundation (NSF). Lead in the environment. Washington,
DC: National Science Foundation; 1977. 272 p.
Nehring, R.B. Aquatic insects as biological monitors of heavy metal
pollution. Bull. Environ. Contain. Toxicol. 15:147-154; 1976. (As cited
by Wong et al. 1978)
Ohi, G.; Seki, H.; Akiyama, K.; Yagyu, H. The pigeon as a sensor of
air pollution. Bull. Environ. Contam. Toxicol. 12(l):92-98; 1974.
6-27
-------
Ozoh, P.T. Malformations and inhibitory tendencies induced Brachydanio
rerio_ (Hamilton-Buchanan) eggs and larvae due to exposures in low con-
centrations of lead and copper ions. Bull. Environ. Contain. Toxicol.
21:668-675; 1979a.
Peterson, P.J. Lead and vegetation. Nriagu, j.o. ed. The biogeo-
cnemistry of lead in the environment. New York, NY: Elsevier-North
Holland Biomedical Press; 1978.
Phillips, G.R. ; Russo, R.C. Metal bioaccumulation in fishes and aquatic
invertebrates: a literature review. Report No. EPA-600/3-78-103.
Washington, DC: U.S. Environmental Protection Agency; 1978.
Pickering, Q.H.; Henderson, C. The acute toxicity of some heavy metals
to different species of warmwater fishes. Air Water Pollut. Int. J.
10:453-463; 1966. (As cited by U.S.EPA 1978)
Pietilainen, K. In: International conference on heavy metals in the
environment; 1975 October 27-31, Toronto, Ontario; 1975: C-279-C-281
(extended abstract). (As cited by Wong _et _al. 1978)
Portmann, J.E.; Wilson, K.W. The toxicity of 140 substances to the brown
shrimp and other marine animals. Shellfish Information Leaflet No. 22.
Conway, N. Wales: Ministry of Agriculture; 1971: 1-2. (As cited by
Forbes and Sanderson 1978)
Quortroup, E.R.; Shillinger, J.E. 3000 wild bird autopsies on western
lakes areas. J. Am. Vet. Med. Assoc. 99:382-387; 1941. (As cited by
Forbes and Sanderson 1978)
Rolfe, G.L.; Haney, A. Inst. Environ. Stud. Urbana, IL: University
of Illinois; 1975: 133 p.
Schell, W.R.; Barnes, R.S. Rubin, A.J. ed. Aqueous environmental
chemistry of metals. Ann Arbor, MI: Ann Arbor Science; 1974: 129-169.
Siegel, S.M.; Eshleman, A.; Umena, I.; Puerner, N.; Smith, C.W. The
general and comparative biology of toxic metals and their derivatives:
mercury and lead. Buhler, D.R. ed. Mercury in the western environment.
Proceedings workshop; 1971 February 25-26, Portland, OR; 1973: 119-
134. (As cited by Bell et al. 1979)
Spehar, R.L.; Anderson, R.L.; Fiandt, J.T. Toxicity and bioaccumulation
of cadmium and lead in aquatic invertebrates. Environ. Pollut. 15:195-
208; 1978.
Tansy, M.F.; Roth, R.P. Pigeons: a new role in air pollution. J. Air
Poll. Control Assoc. 20(5):307-309; 1970. (As cited by U.S. EPA 1977)
U.S. Environmental Protection Agency (U.S.EPA). Air quality criteria
for lead. Washington, DC: U.S. Environmental Protection Agency; 1977.
6-28
-------
I
I
I
I
I
I
1
I
1
I
1
I
I
I
I
I
I
I
I
U.S. Environmental Protection Agency (U.S. EPA). Lead ambient water
quality criteria. Washington, DC: Office of Water Regulations and
Standards, U.S. Environmental Protection Agency; 1978.
U.S. Environmental Protection Agency (U.S. EPA). Monitoring and Data
Support Division Data Files, Office of Water Regulations and Standards;
1979.
U.S. Environmental Protection Agency (U.S.EPA). Lead ambient water
quality criteria for lead. Report No. EPA 440/5-80-057. Washington, DC:
Office of Water Planning and Regulations, U.S. Environmental Protection
Agency; 1980.
U.S. Fish and Wildlife Service (U.S.FWS). Proposed use of steel shot
for hunting waterfowl in the United States. Final environmental state-
ment. Washington, DC: U.S. Fish and Wildlife Service; 1976.
U.S. Fish and Wildlife Service (U.S.FWS). Environmental assessment:
non-toxic regulations for hunting waterfowl, 1980-81. Washington, DC:
U.S. Department of the Interior; 1980.
Varanasi, U.; Markey, D. Effect of calcium on retention of lead in fish
skin. Fed. Proc. Fed. Am. Soc. Exp. Biol. 36(3):772; 1977. (As cited
by Phillips and Russo 1978).
Warnick, S.L.; Bell, H.L. The acute toxicity of some heavy metals to
different species of aquatic insects. J. Water Poll. Control Fed.
41:280-284; 1969. (As cited by Kemp £t al. 1973)
Weir, P.A.; Hine, C.H. Effects of various metals on behavior of
conditioned goldfish. Arch. Environ. Health 20:45-51; 1970.
Weis, P.; Weis, J.S. Effects of heavy metals on fin regeneration in
the killifish, Fundulus heteroclitus. Bull. Environ. Contam. Toxicol.
16(2):197-202; 1976.
Whitley, L.S. The resistance of tubificid worms to three common pollu-
tants. Hydrobiol. 32:193-205; 1968.
Whitley, L.S.; Sikora, R.A. The effect of three common pollutants on
the respiration rate of tubificid worms. J. Water Poll. Control Fed.
42(2):R57-R66; 1970.
Wilkins, D.A. A technique for the measurement of lead tolerance in
plants. Nature 180(4575):37-38; 1957. (As cited by Bell et al. 1979)
Williamson, P.; Evans, P.R. Bull. Environ. Contam. Toxicol. 8:280-288;
1972. (As cited by Forbes and Sanderson 1978)
6-29
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Wong, P.T.S.; Silverberg, B.A.; Chau, Y.K.; Hodson, P.V. Lead and the
aquatic biota. Nriagu, J.O. ed. The biogeochemistry of lead in the
environment. New York, NY: Elsevier-North Holland Biomedical Press;
1978.
Zitco, V. In: Andrew, R.W.; Hodson, P.V.; Konasewich, D.E. eds.
Toxicity to biota of metal forms in natural water. Proceedings work-
shop; 1975 October 7-8, Duluth, MN; 1976: 9-32.
6-30
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7.0 RISK CONSIDERATIONS
7.1 HUMANS
7.1.1 Introduction
The preceding sections presented a discussion of the pathways of
exposure and effects of lead on humans. This section identifies the
subpopulations at risk. Section 5.2, which makes numerous assumptions
about concentrations and consumption, describes exposure scenarios for
certain subpopulations. Although this approach is useful for determining
the relative importance of exposure routes for different subpopulations,
it is not generally useful for evaluating potential risk. Because most
of the observations of effects are correlated with levels of lead in the
blood, measurements of such levels are currently the most appropriate
way to evaluate potential risk.
Given a large enough sample population, levels of lead in the blood
appear to show a log-normal distribution. In certain cases, such as in
urban and smelter areas, this distribution is shifted, which results in
a higher percentage of the population with a given level of lead in the
blood. In addition, there is a wide range in exposure and thus blood
levels at which persons are affected by lead depending on such things as
age, sex, and nutritional status.
A summary of the blood lead levels at which adverse affects of lead
have been observed in humans is shown in Table 7-1. The lowest reported
effect level represents a value at which only a small proportion of the
population is affected. However, the U.S. EPA (1977) developed dose-
response curves that showed a sharp rise in the sigmoid dose-response
curve for the percent of the population affected at only slightly higher
blood lead levels. The no-effect levels are somewhat generalized and
represent levels at which no effects were generally observed. However,
recent studies suggest that subtle neuro-behavioral effects occur at
blood lead levels for which no overt symptoms of lead toxicity are seen.
Available studies on the carcinogenic and mutagenic effects of lead
are inappropriate for risk estimations. Although human data on the
carcinogenicity of lead are scant, no evidence suggests that lead is
carcinogenic to humans. A few feeding experiments with rodents have
resulted in elevated incidences of renal tumors. However, if these
dietary levels were extrapolated to humans, it would require consumption
of 550 mg of elemental lead per day, which is far in excess of the
maximum tolerated dose of lead in humans. Mutagenicity data are also
inconclusive and contradictory.
Damage to the central and peripheral nervous systems and particularly
to the brain, damage to the kidneys, adverse effects on reproductive
capability, and the inhibition of the blood forming process are of con-
siderable concern. Children, because of enhanced absorption and a variety
of other factors, generally exhibit the adverse effects associated with
lead exposure at lower blood lead levels (PbB) than adults.
-------
TABLE 7-1. ADVERSE EFFECTS OF LEAD ON HUMANS'
Adverse Effect
Carcinogenesis
Mutagenesis
Impaired Spermatogenesis
Fetotoxicity
Encephalopathy
Noticeable Brain
Dysfunction
Peripheral Neuropathy
Nephropathy
Reversible
Anemia
Elevated FEP (free
erythrocyte proto-
porphyrin)
Lowest Reported Effect
Level
(ug PbB/100 ml)
50
30-40
80—children
100—adults
50-60—children
50-60
40—children
50—adults
50-60—adults
15-20—children
and women
25-30—men
Elevated ALA (6-amino- 40
levulinate acid) in urine
No-detected-effeet-Level
(ug PbB/100 ml)
> 40 occupational
40-120 occupational
23-41
60—children
> 80—adults
50—children
40
40—children
50—adults
20—children and
women
25—men
< 40
ALAD (6-aminolevulinate
dehydratase) 10 < IQ
Taken from data presented in Section 5.1.
Note that recent studies suggest that subtle neuro-behavioral effects
occur at blood-lead levels for which no overt symptoms of lead toxicity
are seen.
7-2
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The first indication of lead exposure is the inhibition of heme,
the prosthetic group of hemoglobin responsible for oxygen transport.
Inhibition of ALAD, the enzyme responsible for the synthesis of a pre-
cursor to heme, generally occurs at blood lead levels below 20 ug/100 ml.
Several other steps in hemoglobin synthesis are also disrupted at PbB
levels between 20 and 60 ug/100 ml. Mild anemia may occur in adults at
or slightly above PbB values of 50 yg/lOO ml and at a somewhat lower
value (PbB=40 ug/100 ml) in children. Although these effects on heme
synthesis are reversible, the implications of prolonged exposure to these
effect levels are unknown.
Several studies indicate that sublethal lead exposures (PbB=30-40 yg/
100 ml) may impair normal reproductive ability. Alterations in sperma-
togenesis are associated with lead exposure; available data, however, are
limited to high occupational exposures (PbB=50-80 yg/100 ml); therefore,
it is difficult to extrapolate to more typical exposure levels. Absorbed
lead also crosses the placental barrier and enters the fetal bloodstream.
Umbilical blood lead measurements indicate similar levels to those found
in maternal blood. However, increased sensitivity of the fetus to PbB
levels suggests that neurological damage can occur in the fetus with no
overt symptoms of lead intoxication in the mother. No data suggest that
lead is teratogenic in humans.
In addition, a major concern is the capability of lead to induce
irreversible injury to the renal and nervous systems. Kidney disease
associated with chronic lead exposure has not been adequately studied.
Routine clinical tests are ineffective for early diagnosis and irreparable
damage is sustained before chronic lead nephropathy is detected. Advanced
lead nephropathy results in hypertension, interstitial fibrosis, and
eventually reduced glomerular filtration, which progresses into renal
failure. Reduced glomerular filtration occurs at relatively low blood
lead levels (PbB=48-98 yg/100 ml).
Among the most devastating effects of increased lead absorption are
the effects produced on the central and peripheral nervous systems.
Manifested as encephalopathy, effects on the central nervous system are
seen more frequently in children (PbB=80 yg/100 ml) than adults
(PbB=100 yg/100 ml). The minimal level of lead exposure associated
with lead encephalopathy, however, is not clearly known. Effects of
lead exposure in the peripheral nervous system have also been documented.
Peripheral neuropathy affects motor neurons and are characterized by loss
of nerve fibers and segmental demyelination. The lowest reported PbB
levels associated with these effects are 50-60 yg/100 ml.
7-3
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Perhaps of greater societal concern are recent reports of subtle
impairment of the cerebral function in children at PbB levels around
40 ug/100 ml. Many of these studies, as discussed in Section 5.1,
are controversial; flaws in experimental design, complications of
nutritional and socioeconomic status, insensitivity of behavioral tests,
etc. complicate the issue. Despite the problems inherent in these
studies, sufficient evidence exists to indicate that subtle neurobeha-
vioral effects do occur in children exposed to sub-encephalopathic
levels (PbB=40-80 ug/100 ml) of lead. The minimal level of lead expo-
sure, duration, and age of greatest susceptibility cannot be defined
with any degree of certainty at this time.
The exposures of various subpopulations as indicated by levels of
lead in the blood are shown in Table 7-2. Because the data on blood
levels are voluminous, this table presents only a few representative
examples and is not all inclusive. The background information required
for the interpretation of both Tables 7-1 and 7-2 is found in
Sections 5.1 and 5.2. In addition, the actual exposure levels that may
result in the levels of lead in the blood shown in Table 7-2 are dis-
cussed in Section 5.2. Because of the complexity of the toxicology and the
exposure pathways for lead, this section, which is a discussion on the
risk implications for various subpopulations as shown in Tables 7-1 and
7-2, should only be considered in conjunction with Chapter 5.0.
7.1.2 Adults
In general, food is thought to be the major exposure route of adults
to lead (see Section 5.2). The total absorbed dose has been estimated
to be 10-25 yg/day in rural areas. The mean blood levels of lead
in these areas is around 10-ld_yg/100 ml (see Table 7-2). In urban
areas, when exposure via inhalation is more significant, total absorbed
dose is estimated to be 15-40 yg/day. Mean levels of lead in the blood
are about 15-24 yg/1. Persons living near smelters or other lead
industries are exposed to higher levels of lead (about 70-300 yg/day
as an absorbed dose), and a sizeable segment of the population show a
blood level of greater than 40 yg/100 ml.
Although Table 7-2 does not identify the isolated subpopulations
that can be exposed to high levels of lead, these have been discussed
in Section 5.2. These subpopulations include those persons who consume
drinking water that is highly contaminated resulting from the use of
lead pipes, contaminated moonshine whiskey, and excessive amounts of
contaminated wines. Of these population groups, the first two are likely
to be larger than the group exposed to lead through contaminated wines.
In addition, certain segments of the population are particularly
susceptible to lead exposure. For example, calcium and iron deficien-
cies, commonly observed in pregnant women, place them at a higher risk
to lead toxicosis. In addition, Calabrese (1978) noted that individuals
with latent porphyria may develop clinical symptoms when exposed to
elevated levels of lead.
7-4
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TABLE 7-2. HUMAN EXPOSURE TO LEAD AS EVIDENCED BY BLOOD
LEVELS IN THE UNITED STATES
Location
Adults
Rural/Urban
Urban
Rural
Within 3.7 meters of
Highway
Living Near a.Smelter
Children
Urban (primarily)
Within 30 meters of
Highway
Near Smelter—Kellogg,
ID—1974 (immediate
vicinity)
1975
1979
El Paso, TX
Blood Level
(yg/100 ml)
9-24
Most ^ 16
Reference
Bell et al. (1979)
18—mean (adjusted Tepper and Levin (1972)
for age and smoking)
Less than 5% > 30
16—mean (adjusted
for age and smoking)
Less than 0.5% > 30
23—mean Daines et al. (1972)
16% >40
40,000 children de-
tected annually
> 30
^20 yearly geo-
metric mean
50% > 40
99% > 40
60% > 60
Somewhat reduced'
Almost all < 60?
and most < 40
70% > 40
14% > 60
Landrigan et al. (1975)
Billick e± al. (1980)
Caprio et al. (1974)
Walter £t al. (1980)
Anonymous (1979)
Landrigan et_ al. (1975)
Reduction as a result of reduced atmospheric emissions as well as
increased sanitary procedures for the workers who were apparently
exposing their children to lead through their clothing.
7-5
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Thus, a relatively large portion of the adult population is exposed
to^levels of lead that might result in some inhibition of heme synthesis.
Efrects on renal function and nervous systems are a potential risk to a
much smaller subpopulation and are limited, for the most part, to occupa-
tional exposure. Impaired reproductive capacity has not been well studied-
however, it does represent a potential risk to adults.
7.1.3 Children
Children are exposed to high levels of lead in numerous situations
(see Table 7-2 and Section 5.2). Large numbers of children in urban
areas, in rural areas where lead paint has been used, near highways.
and near lead industries show levels of lead in blood greater'than
30 ug/100 ml. Levels greater than 60 yg/100 ml are also not uncommon
in children living in or near these areas.
The fetus, infant, and child have all been demonstrated to be
especially susceptible to lead (see Section 5.1). At least to some
portion of the subpopulations described in the previous paragraph,
current exposure levels can result in anemia, irreparable damage to
kidneys and motor neurons, noticeable brain dysfunction and encetmalo-
pathy.
Needleman (1980) discusses the problems of lead in children in the
United States today. He points out that subtle effects on such things
as learning capacity and number of synapses are being reported at
increasingly lower exposures. The age of exposure appears to be especi-
ally important in effects observed later in life. Although studies in
this area are controversial and somewhat contradictory, available evi-
dence suggests cognitive impairment and behavioral effects in children
with PbB concentrations consistently over 40 yg/100 ml. While some data
indicate effects below this value, the evidence to date is inconclusive.
In addition, he describes studies that suggest children who had apparently
recovered from acute lead intoxication still showed behavioral disorders
and sensory motor defects.
Thus, the preceding sections and most of the authorities on the
subject (e.g., Needleman 1980, Mahaffey 1978) suggest that exposure to
lead still represents a risk to children in the United States. The
phasing out of lead in gasoline, the elimination of lead paint, the
treatment of existing painted surfaces, controls on lead air emissions,
especially from lead smelters, and the reduction of the use of lead
solder in canned foods are expected eventually to greatly reduce the
exposure of children to lead. However, the problem will continue for
some time because of the existing contaminated soils and houses where
lead paint was used.
7.2 RISKS TO BIOTA
7-2.1 Aquatic Organisms
Very few instances have been reported of fish kills attributed to
lead; however, this is not a reliable measure of the risk that lead poses
7-6
-------
to aquatic organisms. Chronic exposure to sublethal levels of lead may
cause subtle yet significant harm to aquatic ecosystems, particularly
in areas near anthropogenic sources of lead. To assess the risk of
aquatic organisms with regard to lead, one can compare the concentrations
that have resulted in effects in the laboratory with those concentrations
that have been observed in the environment to cause effects.
The ranges of lead concentrations causing sublethal and lethal
effects in various aquatic species as determined in laboratory studies
are summarized below. The data supporting these conclusions are described
in detail in Section 6.1.
• <10 yg/1 Life-cycle toxicity test in soft water produced
abnormal development in rainbow trout. All
other species tested are unaffected.
• 10-100 yg/1 Sublethal effects reported for several freshwater
fish species in soft water, as well as growth
inhibition in sensitive freshwater algae.
Chronic toxicity reported in soft water are
based on effects on early life stages in fish
and life cycle tests in Daphnia.
• 100-1000 yg/1 Sublethal toxicosis in a variety of freshwater
fish and invertebrates in soft and moderately
hard water. Acute effects were observed on
stickleback and some invertebrates. Numerous
species of freshwater algae adversely affected,
as well as more sensitive marine microflora.
• 1.0-10.0 mg/1 Acute toxicity level for several freshwater fish
and invertebrate species in soft water and for
sensitive marine invertebrates. Algicidal for
some marine algae.
• 10.0-100 mg/1 Acute effects observed in a variety of freshwater
fish and in most invertebrates tested. All algae
species tested sensitive in this range.
• >100 mg/1 Only the most resistant species (e.g., red
shiner, mosquitofish, cockle) are able to
survive even for short periods in this range
of concentrations. Hard water would be impor-
tant for tolerance to such elevated levels.
7-7
-------
This summary is intended only as a general guide in the assessment
of the ecological impact of a given lead concentration in an aquatic
environment.
Surface water concentrations of lead included in the STORET data
base and from other miscellaneous sources are summarized in Table 7-3.
The concentrations and their geographical distribution are discussed in
more detail in Sections 4.2 and 6.2. For at least one year between 1975
and 1979, seven of the 18 major continental U.S. river basins designated
by STORET have had mean total lead levels exceeding 50 ug/1 ~ a level
indicating possible chronic toxicity in some species (see monitoring data
in Chapter 4.0). Of these basins, only the Great Basin exceeded this
level in 1979. Also, as indicated in Section 6.1, the levels of exposure
increased in acidic or soft waters as a result of the increased availa-
bility of lead for uptake. In general, risk of exposure increases in
basins with soft water, such as New England, the Pacific Northwest, and
the Southeast.
From the limited data presented, it appears that the ambient con-
centrations occasionally reach levels of concern for most aquatic species.
Source-specific locations, such as mining areas or in streams receiving
urban runoff, may achieve lead concentrations potentially eliciting sub-
lethal and lethal effects in both invertebrate and fish species. The
U.S. EPA water quality criteria are exceeded in numerous locations.
Comparing monitoring data of lead concentrations in natural waters
and effects levels to aquatic organisms in laboratory studies, hox^ever,
can be a problem. Monitoring studies report total lead levels while
suspended lead is not generally a consideration in laboratory studies.
A large portion of the total lead in natural systems is bound to parti-
culate matter (see Section 4.2). Only conjectures can be made about
the percentage of bound lead and the role this fraction plays in lead
toxicity. Some potential for re-release to the water column always
exists, although Chapter 4.0 suggests that lead is tightly bound. With-
out information on the ambient levels and distribution of completing
agents, such as organic and inorganic ligands, suspended sediment levels,
changes in pH (resulting from spring floods, acid rain) and the influences
of industrial effluents on the dynamics of adsorption and complexing, no
estimates of actual or potential lead availability to biota can be made.
In addition, the role of ingestion of sediment lead and its transfer up
the food chain is not well understood. The data have been presented to
illustrate: (1) the prevalence of ambient concentrations exceeding
levels that have adverse effects on certain aquatic species in the labora-
tory, and (2) specific situations where lead concentrations occur that may
have adverse effects on most aquatic life.
7-8
-------
TABLE 7-3. CONCENTRATIONS OF LEAD IN WATER
Total Lead
Source Concentration
STORET — Ambient levelsa
7.7% of U.S. minor river basins have a
mean concentration exceeding this level 50 ug/1
8.1% of U.S. minor river basins have 10%
of maximum concentrations exceeding this level 100 ug/1
Miscellaneous Source-related Levels
Mine wastewater, Yukon Territory 1000 ug/1
Boyle (1965)
Settling pond, mine in MO 1000 ug/1
Proctor _ejc _al. (1974)
Mine and creek waters in mining area, U.S.S.R. 7000 - 9000 ug/1
Edgington and Robbins (1976)
Stream near lead smelter, MO 300 ug/1
(Gale and Wixson 1979)
Storm runoff wastewater in Durham, NC 100 - 12,000 ug/1
(Chow 1978)
Runoff from streets of high traffic density
in Oklahoma City, OK 5500 ug/1
(Chow (1978)
Sewage effluent in city with lead-emitting 100 _ 50Q u /-,
industries ~ g
(Chow (1978)
Sewage effluent in Los Angeles, CA 250 ug/1
Chow (1978)
3Data described in greater detail in Table 6-5.
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7.2.2 Terrestrial Organisms
7.2.2.1 Mammals
The risk of exposure to lead in toxic concentrations is apparently
greatest for relatively nonmobile species that live near anthropogenic
sources of lead. Most studies on lead poisoning in mammals have focused
on rodents living various distances from a highway. Clark (1979) has
observed mortality in laboratory tests on domestic mammals at daily
doses of 1 to more than 10 mg/kg/day. The same author estimated that
daily lead doses range from 1 to 128 mg/kg/day for wild rodents and
insectivores (e.g., shrews) living near highways. Elevated tissue
residues have been observed in specimens living near roadsides; however,
there have been no reports of lead poisoning from this type of exposure.
Robert and co-workers (1978) found renal inclusions and edema in
rodents living near abandoned mines in Wales, and attributed the effects
to high lead burdens (8-45 mg/kg dry weight). Haschek and co-workers
(1979) examined rodents living in an orchard that had been treated
earlier with lead arsenate. Several specimens had renal damage, which
the authors thought was associated with high residues of 14 mg/kgi
(dry weight) in the kidneys. Soil concentrations in the area averaged
1342 mg/kg (dry weight).
Grazing animals, such as deer, may be exposed to higher levels
because they frequently forage near roads. Some evidence suggests
that lead does not biomagnify in food chains (Williamson and Evans 1972),
although this does not necessarily imply that carnivores are not at
risk.
Because the relationship between tissue residues and toxicity is
not clear, it is impossible to assess the risk to various species on
the basis of lead concentrations in tissues. Nonetheless, body burdens
do reflect elevated exposure in some areas and may be a measure of
potential risk.
7.2.2.2 Birds
According to numerous reports of lead poisoning in birds, the vast
majority of mortalities occurs in waterfowl as a result of ingested
spent lead shot. Yearly, losses of waterfowl (from lead poisoning)
were estimated at 2-3 million birds, or 2-3% of the U.S. waterfowl
population (Bellrose 1959); more recent nationwide figures were not
available.
The risk of lead poisoning from shot ingestion is most closely
associated with the hunting pressure in a given area. Of the four
major flyways in the United States, the Mississippi had 40-45% of the
total waterfowl hunting activity. Approximately 25% of the hunter-days
took place in the Central Flyway, while the Atlantic and Pacific each
had less than 20% (Bellrose 1959).
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Certain species of waterfowl are much more likely to ingest lead
shot than others, largely because of feeding habits. Among several
surveys of gizzard contents from bagged birds (U.S. FWS 1976), diving
ducks had the highest incidence of ingested shot. In this group
canvasback, redhead, scaup, and ring-necked ducks appear to be at
the highest risk because they have the greatest tendency to ingest lead
shot. Other species of special concern are waterfowl that consume corn
as a major component of the diet. These include the Canadian geese,
mallard, pintail, and related species of dabbling ducks.
In 1976, the U.S. Fish and Wildlife Service began a gradual
phasing-out of the use of lead shot for waterfowl hunting. By the
fall of 1980, lead shot was completely prohibited for all types of
shotguns in certain areas that account for about 20% of the waterfowl
harvest of the United States (U.S. FWS 1980). In states that have
aggressively promoted the use of nontoxic steel shot as a substitute,
some promising results have been achieved. At the Sauvie's Island
State Management Area in Oregon, 5000-6000 mallards perished each year
from lead poisoning before lead shot was prohibited. For several years
after the regulation requiring steel shot, mallard mortality as a
result of lead ingestion decreased 25% per year. Officials'at Turk's
Pond in Colorado reported a "pronounced change" in goose mortalities
after the use of steel shot became mandatory. In Michigan, lead shot
has been selectively prohibited. Smith (1980) noted that 50% of
the shot now found in waterfowl gizzards is steel. From this evidence,
it seems likely that the continued phase-out of lead shot will further'
reduce the incidence of lead poisoning in waterfowl.
Other species of birds may also ingest lead shot accidentally during
feeding. Of these, the species with perhaps the highest rate of lead
shot ingestion are doves. In an examination of doves bagged by hunters
Lewis and Legter (1968) found lead shot in 1% of the gizzards. Aquatic*
predators, such as ospreys and bald eagles, are also at risk to the
extent that they feed on animals containing lead shot (U.S FWS 1980
Bagley and Locke 1967). '
Like other organisms, birds in urban areas tend to have higher
lead residues in their tissues than populations in rural areas.
Possible sources of lead exposure to urban birds include dirt and air
pollution. The ingestion of tailings from lead mine wastes has led
to death in waterfowl on several occasions; therefore, the risk of
lead poisoning is probably somewhat higher in mining areas than other
areas.
7.2.2.3 Plants
It is extremely difficult to relate effects data to exposure
levels in order to estimate environmental risk for plants. In
laboratory experiments, lead is usually presented as a salt in aqueous
solution or in vapor form (Section 6.1). However, with these exposure
techniques, the observed effects levels are not equivalent to concentra-
^°™ av^lable for uPtake from soil. For example, lead concentrations
of 30 mg/1 reduced corn seedling growth in a nutrient culture, but
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had no effect when present at 270 mg/1 in soil (Tornabene e_t al. 1977)
In field toxicity studies, the factors influencing biological availa-
bility are unknown; thus, generalization from the results to other
situations and conditions is impossible.
in «]?? 1t'S"tUre d06S n0t contain reP°«s of lead poisoning to plants
in field situations. However, indirect effects on productivity (± e
delay nutrient recycling because of microbial inhibition) haJe been
observed within one-half mile of a lead smelter.
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REFERENCES
Anonymous. Lead in canned food to be reduced. Chemical and Engineering
News 57(37) :20; 1979.
Bagley, G.E., Locke, L.N. Bull. Environ. Contam. Toxicol. 2:297-305;
1967. (As cited by Forbes and Sanderson 1978)
Bell, M.A. ; Ewing, R.A. ; Lutz, G.A. ; Holoman, V.L.; Paris, B.;
Krause, H.H. ; Hammond, P.B. Reviews of the environmental effects of
pollutants: VII. Lead. Report No. EPA-600/1-78-029. Columbus, OH:
U.S. Environmental Protection Agency; 1979. 476 p. Available from:
NTIS, Springfield, VA; PB80-12107 2.
Bellrose, F.C. Lead poisoning as a mortality factor in water populations.
111. Nat. Hist. Surv. Bull. 27(3) : 235-288; 1959. (As cited by U.S. Fish
and Wildlife Service 1976)
Billick, I.H. ; Curran, A.S.; Shier, D.R. Relation of pediatric blood
lead levels to lead in gasoline. Environ. Health Persp. 34:213-217-
1980.
Boyle, R.W. Can. Dept. Mines and Tech. Surveys. Geol. Survey Bull.
Ill; 1965. (As cited by Nriagu 1978)
Calabrese, E.J. Will elevated levels of lead exposure precipitate
clinical symptoms of porphyria in individuals with the latent condition?
Medical Hypotheses 4:282-289; 1978.
Caprio, R.J. ; Margulis, H.L.; Joselow, M.M. Lead absorption in children
and its relationship to urban traffic densities. Arch. Environ. Health
28:195-197; 1974. (As cited by U.S. EPA 1977)
Chow, T.J. Lead in natural waters. Nriagu, J.O., ed. The biogeochemistry
of lead in the environment. New York, NY: Elsevier North Holland
Biomedical Press; 1978.
Clark, D.R. Lead concentrations: bats vs. terrestrial small mammals
collected near a major highway. Environ. Sci. Technol. 13(3) .-338-341-
1979. '
Daines, R.H. ; Smith, D.W.; Feliciano, A.; Trout, J.R. Air levels of
lead inside and outside of homes. Ind. Med. and Surg. 41:26-28- 1972
(As cited by U.S. EPA 1977)
Forbes, R.M. ; Sanderson, G.C. Lead toxicity in domestic animals and
wildlife. Nriagu, J.O. , ed. The biogeochemistry of lead in the
environment. New York, NY: Elsevier North Holland Biomedical Press-
1978.
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Gale, N.L.; Wixson, B.C. Cadmium in forest ecosystems around lead
smelters in Missouri. Environ. Hlth. Perspec. 28:23-37; 1979.
Haschek, W.M.; Lisk, D.J.; Stehn, R.A. Accumulations of lead in rodents
from two old orchard sites in New York; 1979. In: National Academy of
Sciences (ed.). Animals as monitors of environmental pollutants; 1979.
Landrigan, P.J.; Gehlbach, S.H.; Rosenblum, B.F.; Shoults, JM •
Candelaria, R.M.; Barthel, W.F.; Liddle, J.A.; Smrek. A.L.;
Staehling, N.W.; Sanders, J.D.F. Epidemic lead absorption near an
— smelter: the role of particulate lead. New Eng. J. Med. 292:123-
; 1975. (As cited by U.S. EPA 1977)
Lewis, J.C.; Letger, E.J. Wildlife Manag. 32:476-482; 1968. (As cited
by Forbes and Sanderson 1978)
Mahaffey, K.R. Environmental exposure to lead. Nriagu, J.O. ed The
biogeochemistry of lead in the environment. New York, NY: Elsevier
North Holland Biomedical Press; 1978: Chapter 11, 1-36.
Needleman, H.L. ; Gunnoe, C. ; Leviton, A.; Reed, R. ; Peresie H •
Maher, C. ; Barrett, P. Deficits in psychologic and classroom perfor-
dentine lea<* levels. New Eng. J. Med.
Needleman, H.L. Lead exposure and human health: recent data on an
ancient problem. Tech. Rev. 39-45; March/April 1980.
Nriagu, J.O. ed. The biochemistry of lead in the environment. Part A
New York, NY: Elsevier/North-Holland Biomedical Press; 1978.
Proctor, P.O.; Kisvarsanyi, G. ; Garrison, E. ; Williams, A. In: Trace
substances in environmental health VII. D.D. Hemphill (ed.). Columbia,
«0: University of Missouri; 1974:57-61. (As cited by Chow 1978)
Smith, R. Personal communication. Migratory Bird Management Office-
U.S. Fish and Wildlife Service; 1980.
Tepper, L.B.; Levin, L.S. A survey of air and population lead levels
in selected American communities. Final report. Seven cities study.
Cincinnati, OH: University of Cincinnati, College of Medicine- 1972
(As cited by Bell et al. 1979)
Tornabene, T.G. ; Gale, N.L.; Koeppe, R.L.; Zimdahl, R.L. ; Forbes, R.M.
Microorganisms, plants, and animals. In: W.R. Boggess and B.C. Wixson
(eds.). Lead in the environment. NSF/RA-770 214.
U.S. Environmental Protection Agency (U.S. EPA). Air quality criteria
for lead. Report No. EPA-600/8- 77-017. Washington, DC: Office of
Research and Development; 1977. Available from: NTIS , Springfield, VA;
PB 280 411.
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U.S. Fish and Wildlife Service (U.S. FWS). Non-toxic shot regulations
for hunting water fowl, 1980-1981. Washington, DC: U.S. Fish and
Wildlife Service; 1976.
Walter, S.D.; Yankel, A.J.; von Lindern, I.H. Age-specific risk factors
for lead absorption in children. Arch. Environ. Health 35:53-58; 1980.
Williamson, P.; Evans, P.R. Bull. Environ. Contain. Toxicol. 8:280-288;
1972. (As cited by Forbes and Sanderson 1978)
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APPENDIX A. NOTES ON THE DERIVATION OF TABLE 3-1
1. Information on lead supplies were derived from the Mineral Commodity
Profiles for 1977 (U.S. Bureau of Mines 1977a).
2. Consumption data are from Lead Industries Association, Inc. (1978), and
from statistics compiled by the American Bureau of Metal Statistics
(Kirk-Othmer 1967).
3. According to Nriagu (1978), the following emission factors apply to
the mining and milling of lead ores on a global basis for 1974 and
1975:
mining 0.91 kg/kkg
milling 1.32 kg/kgg
Total 2.23 kg/kkg
Assuming an airborne emissions capture rate of 50% for U.S. mining
and milling operations, the effective total emission factor is 1.12
kg/kkg of lead mined and milled domestically (517,897 kkg); this
corresponds to an airborne emission for domestic mining and milling
of 580 kkg. To this must be added the airborne emission from the
smelting and refining of domestic ore concentrates, a process for
which Nriagu (1978) gives a worldwide emission factor of 6.36 kg/kkg;
however, assuming an emissions capture rate of 75% in domestic
smelting and refining operations in 1976, the effective emission
factor for smelting and refining is 1.59 kg/kkg for which the air-
borne emission would be 823 kkg. Thus, the total airborne emission
from the mining, milling, smelting, and refining of domestic ores
is 1403 kkg. The solid wastes that result from emissions capture
are reflected in the solid waste emission level for the category
of primary domestic lead production.
4. Imported ores must be smelted and refined in the United States.
Nriagu (1978) assigns an emission factor of 6.36 to the worldwide
smelting and refining of lead. In the United States, some of the
airborne emissions are captured; and if the emissions capture rate
is taken to be 75%, then the effective emission factor is 1.59 kg/kkg.
The amount of lead refined from imported ores was 78,909 kkg in 1976,
which corresponds to an airborne emission of 125 kkg.
The emissions that are captured, 75%, are assumed to show up in the
solid waste stream for the category of imported ores that are domes-
tically smelted and refined, or 375 kkg.
5. The airborne emission volume of 184 kkg associated with secondary
lead production is derived on the basis of an emission factor of
0.35 kg/kkg of secondary lead produced (U.S. EPA 1974). The amount
of secondary lead produced was 526,060 kkg in 1976; therefore, the
air emission was 184 kkg.
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No data are available concerning airborne emissions from battery
production. However, in the production of batteries, grids and'
posts are cast, which may give rise to losses via volatilization
(U.S. EPA 1975, 1976). Material handling may also contribute to
airborne emissions. Using the emission factor of 0.5% (see note
10) of the lead used in smelting and casting, the estimated air-
borne emissions from battery production is about 1700 kkg. With
regard to lead oxide used in batteries, airborne emissions might
be associated with handling procedures, however, amounts are un-
known; and, if the lead oxide is produced from lead metal, then
emissions could be significant, depending on the amount of emis-
sions capture machinery used to minimize emissions.
Airborne emissions of lead used in gasoline antiknock additives
consist of two components: emissions due to manfuacturing pro-
cesses, which according to data compiled by the Noyes Data
Corporation (Sittig 1975) was 1614 kkg in 1976; and emissions from
the combustion of leaded gasolines, which is taken as 80% of the
217,461 kkg of lead used in antiknock additives (Hepple 1971).
The sum of these two airborne emissions associated with antiknock
additives is 175,584 kkg.
Ammunition is assumed to consist primarily of lead shot and small-
caliber bullets that are steel- and copper-jacketed. The airborne
emission of 666 kkg is based on an assumed air emission factor of
1%, which is evolved during the firing of the round and during the
impact, especially in firing ranges owned by the military, the
police forces, and by private gun clubs. Air emissions during the
manufacture of rounds is possibly even greater than the loss during
actual firing; however, no data are available on which to base an
estimate. The solid waste (land-destined) lead burden associated
with ammunition is assumed to be about 75% of the total amount of
lead used in ammunition; this is attributed to rounds spent in mili-
tary and sport gun use where the rounds are unrecoverable, and to
practice ranges where the spent rounds are not recovered. Losses to
POTWs are considered to be negligible; and lead losses to water, if they
occur at all, probably take place during manufacturing operations.
Air emissions of lead during solder use are estimated to be on the
order of at least 2% of the amount of lead used in solder. The
loss to the air is attributable to volatilization during the solder
use, especially during manual use operations as in plumbing and
electronics repair. Airborne emissions of lead during solder manu-
facture no doubt take place but the amount is unknown and no esti-
mate has been made; also losses to the air during automated soldering
operations are probably minimal because temperatures are automatically
controlled. Aquatic and POTW emissions of lead due to solder use
are probably small, though the amount of lead going to POTWs because
of solder use is probably greater than the amount going directly to
x^aters since solders are used extensively in plumbing systems
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carrying water that ultimately goes to POTWs (though, of course,
many plumbing systems carry water to nonPOTW sinks). The amount
of lead going to land as a result of solder use is taken as 10%
of the total amount of lead used in solder and is assumed to be
primarily due to the disposal of electronic apparatus and losses
of solder during manual soldering use in plumbing and electronics
repair.
10. Airborne emissions of lead during the production of weights and
ballasts is attributed to volatilization losses during melting and
casting. The emission factor is estimated to be on the order of
0.5% of the amount of lead used (20,286 kkg), or about 101 kkg.
Losses to water and POTWs during production and use are unknown,
but are probably an extremely small percentage of the total amount
of lead used in weights and ballasts. Solid losses to the environ-
ment are attributed to the loss and disposal of lead weights in the
form of wheel balance weights and fishing-gear sinkers and are
estimated to be on the order of at least half of the lead used in
the weights and ballast category; i.e., 10,143 kkg to solid waste.
11. Emissions associated with lead pigments are based on emissions
factors taken from the cadmium production and use report for losses
due to cadmium pigment manufacture. Emissions during use processes
are not known, but solid waste associated with packaging disposal,
plus water losses associated with the use of paints and pigments
might be at least equal to the amounts shown below and in Table
3-1. The emission factors derived from the cadmium production
and use report (Versar 1980) are as follows (the emission is
based on 15,087 kkg of lead used in pigments):
Emission Factor Emission
(%) (kkg)
Air 1.4 212
Water 0.1 15
POTW 0.3 45
Solid 2.4 363
12. Emissions resulting from the use of 14,449 kkg of lead in 1976 in
lead cable covering is estimated to be 0.1% due to rolling and
handling processes during production, or 14 kkg. Losses to water
are unknown, probably small; and to POTWs the losses are estimated
to be small because of the low solubility of lead in water. Solid
wastes are estimated at about 25%, due to the replacement and
disposal of lead-covered cable in commercial and residential
applications; i.e., about 3612 kkg to land.
13. Air emissions of lead during the manufacture of leaded brasses and
bronzes are estimated at about 5% of the lead used. (The high
volatilization figure is used because of the higher melting tempera-
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ture of brasses and bronzes relative to that of lead.) At 5% the
14,203 kkg of lead associated with brasses and bronzes result in
an airborne emission of 710 kkg. Because lead is added to brasses
and bronzes to improve machineability, significant losses would
occur during machining operations, especially in small shops where
recovery of metal scraps is not consistent. Also, the rate at which
machined brass, and bronze components of consumer goods are disposed
of and replaced by new units, plus the solid losses due to machining
processes, together amount to an estimated 20% of the lead used in
brasses and bronzes, or about 2840 kkg of lead to solid waste.
Losses of lead to water and to POTWs are probably negligible,
especially during industrial and consumer use of leaded brasses
and bronzes. However, the manufacture of leaded brasses and
bronzes might result in some amount of loss of lead to the waters.
14. According to the U.S. Bureau of Mines (1977a), lead sheet is used
in radiation shielding, vibration dampening, and sound attenuation,
the latter category being widely used in modern architecture.
However, lead use in roofing and flashing has decreased, which
means that old buildings that are torn down might be a source of
solid lead wastes. Because sheet lead must be rolled during pro-
duction, an air emission estimate of 0.1% is reasonable, so that the
22.165 kkg of lead used in sheeting accounts for an air emission of
22 kkg; airborne emissions during use of lead sheeting is negligible.
Because lead sheeting is used in industry to protect process vessels,
especially in the handling of highly corrosive materials, some losses
of lead are likely to result in a way that will reach aqueous media;
however, data are unavailable on the amounts of lead sheeting
actually used by industry to protect its process vessels. Generally,
lead losses to the waters and to POTWs due to the manufacture and
use of lead sheet are estimated to be negligible. Solid losses
of lead due to sheeting are estimated to be on the order of at
least 10% of the amount of lead used in sheeting, i.e., 2216 kkg.
15. Lead-alloy bearings are of the "plane" type that operate usually
in a forced lubrication environment of the kind found in automobile
engines and railway car journal boxes. Bearing wear results in
losses of lead to the lubricant, which in turn can be discarded
to land, and a small amount might be disposed of by incineration,
thereby causing an airborne emission of unknown magnitude. The
primary airborne emission assoicated with lead-alloy bearings would
result during the manufacturing process, when it is estimated that
about 0.5% of the lead would be volatilized to the air. Thus, the
air emission from the use of 11,848 kkg of lead in bearings is 59
kkg. Some emission of lead might result to water becasue of the
manufacturing of lead-alloy bearing, however, the amount is unknown
and the amount goint to POTWs during manufacure is estimated to be
negligible. The solid wastes of lead attributable to bearing use
is estimated to be on the order of at least 80% of the amount of
lead used, the rationale being that it is uneconomical to recycle
and recover the lead alloy used in the large amount of steel-backed
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replaceable bearing units; the other 20% of lead use is taken to
account for an increase in the number of lead-alloy bearing in
service and in replacement stocks.
16. The amount of lead used in calking metals was 11,315 kkg in 1976. •
Lead calking is still required, because of its corrosion resistance,
in the building codes of some locales (U.S. Bureau of Mines 1977a).
The manufacture of sheet lead and strips of lead for calking is esti-
mated to result in an airborne emission of 0.1% due to rolling and
handling processes, or a total emission of 11 kkg. Water discharges
due to manufacture are unknown but probably small, as are POTW dis-
charges. Discharge to waters and POTWs during use can be taken as
zero. With regard to solid wastes, lead calking has been used in
buildings for a long time, the discharging of lead from old buildings
that are destroyed must be on the order of at least an estimated
25% of the amount used in manufacturing in 1976, or a total solid
emission of 2716 kkg.
17. Lead pipes, especially traps and "ells" (bends) are still required
by the building codes of some localities (U.S. Bureau of Mines
1977a) was much more common because of the ease of fabrication of
lead pipes and fittings. If a conservative estimate of 0.1% is
taken as the airborne emission factor for the manufacture (rolling,
casting and extrusion) of lead pipe fittings, then the manufacturing
air emission of lead would be about 12 kkg, based on a use level of
12,507 kkg of lead in 1976. Losses of lead to water and POTWs are
unknown and could be a significant portion of the lead used in pipes
and pipe fittings. If the disposal rate of old lead pipes in
buildings that are demolished is taken at 25% of the amount of
lead used in pipes in 1976, then the solid waste volume from lead-
pipe uses is about 3127 kkg.
18. Collapsible tubes are used for the packaging of toothpastes, artists
colors and corrosive chemicals (U.S. Bureau of Mines 1977a).
Because they are manufactured by extrusion, a small amount of
airborne emission can be assumed due to high working temperature
and abrasion with the extrusion dies. An estimated emission
factor of 0.1% means that the manufacturing air emission would
be on the order of 2 kkg (out of the total amount of lead used
in collapsible tubes of 2112 kkg). Emissions to waters and POTWs
can be taken as effectively zero, as far as use is concerned because
the tubes are not exposed to water very much during use, though a
small aqueous discharge might be associated with tube production.
All of the lead uses in collapsible tubes can be assumed discarded
to land, except for a small amount that might find its way to dis-
posal by incineration.
19. The bulk of lead used in printing type is used by the newspaper
industry and related industries where large volumes of materials
must be printed in short periods; situations where photographically
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prepared plates of the kind used in off-set printing would not
have adequate durability for printing upwards of half a million •
impressions. Because "hot-type"linotype machines used melted I
type metal, some losses due to volatilization can be expected,
and because the temperature is precisely controlled, it is likely
that, conservatively, the volatilization losses would be no more I
than that encountered in the controlled temperature melting of •
lead in other automated melting processes, i.e., on the order of
0.5%/yr. Thus, the airborne losses of lead as a result of printing I
operations would be about 68 kkg/yr, based on a total lead use of I
13,611 kkg in 1976. Losses of lead as solid waste from the use of
lead in type would be by means of spills, drips, and adherence of •
small amounts of lead to the disposable cardboard plates into |
which the lead is cast; an estimate of the losses of lead to solid
waste streams as a result of floor sweepings and other loss pro- •
cesses is at least 1%, and probably much higher. At 1% the amount I
is 136 kkg. With regard to water losses, it is considered improb-
able that much lead finds its way into the waters either directly _
or indirectly, however, because most users of hot-type printing •
processes are urban located, any lead losses that do take place •
probably go to POTWs, but in amounts that cannot be estimated.
20. Terne metal is a coating of four parts lead to one part tin and is I
used to coat sheet iron and steel. Because only 1447 kkg of lead
were used in terne metal applications in 1976, the amounts lost to •
the media were probably also small. Because industrial melting p
processes are well controlled, the volatilization losses during
coating processes would be small but probably not less than 0.5%, m
or about 7 kkg. And assuming a disposal rate of 5% the solid I
waste burden from the use of terneplate would be about 72 kkg.
Losses to water and POTWs are considered negligible because of the _
low water solubility of lead and because of the relatively small •
amount of lead used in terne metal. *
21. Baths of molten lead can be used in the annealing of certain alloys, I
The presence of baths of lead in a sustained molten state would be •
expected to account for relatively large volatilization losses,
especially because the effective surface area for volatilization •
would be large as a result of the dipping and withdrawal of hot |
metal parts. Therefore, a conservative estimate of volatilization
losses from annealing processes is on the order of 10%/yr, or 262
kkg of the 2624 kkg of lead used in annealing processes in 1976.
Solid losses due to the adhering of lead to annealed parts, and
the subsequent losses of lead in ways that it would be discarded
along with other solid waste (e.g., as floor drippings, and as
flakings from annealed parts), plus the disposal of lead oxide
scums that form on the surface of baths of lead, must account for
at least 20%/yr of the lead used, or 524 kkg minimum. Losses to
waters and POTWs is estimated to be minimal.
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22. White lead is a term applied primarily to lead carbonate; it is
also used for lead sulfate and lead silicate, and the primary use
is as a pigment in paints. The amount of lead in white lead in
1976 was 2715 kkg. An estimate that is considered conservative
for losses as solid waste due to the production and use of white
lead is 2% due to dust losses that settle out and to losses asso-
ciated with packaging disposal. Because it is likely that some
packaging used by white lead manufacturers to ship the product to
paint formulators is incincerated, a volatilization loss probably
occurs. Estimating the airborne loss at 0.5% and the solid loss
rate at 1.5%, the amount of lead lost to air is 14 kkg and the
amount lost to landfills is 41 kkg; to the latter amount must be
added the amount of painted products that are discarded, which,
assuming a discard loss rate of 10%/yr minimum, the total solid
lead loss rate to land is at least 312 kkg. Losses to waters and
POTWs are unknown, however, it is possible that upwards of 5%
might be lost to aqueous sinks, albeit in a nonsolubilized form,
because lead compounds are not readily soluble in water.
23. Only 350 kkg of lead were used in plating processes in 1976. Losses
to waters and POTWs would probably be small also, however, because
of the lack of data, an estimate cannot be assumed. Airborne losses
are probably negligible, except for losses of lead compounds due to
dusting, which would probably rapidly settle out. Solid losses
due to plating would most likely be in the form of discarded lead-
plated products, however, because of the lack of data, the disposal
rate of plated products cannot be estimated.
24. The amount of lead used in cast products was 6084 kkg in 1976.
Because lead that is cast must be heated to a temperature that is
somewhat higher than its melting point, higher levels of volatiliza-
tion losses can be expected than would result from other manufacturing
processes involving the use of molten lead, as in the manufacture
of ammunition, solder, weights and ballasts; therefore, the volatil-
ization loss rate is estimated to be at least 1% or 61 kkg. Solid
losses due to spilling, and the removal of casting flash, plus any
losses that take place with disposable molds is at least several
percent, which, along with the solid disposal of used cast products,
could be conservatively estimated at 25%, or 1521 kkg. Losses to
waters and POTWs are unknown, but probably only on the order of
several kkg.
25. As with annealing, galvanizing processes involve hot dipping in
molten baths of lead; thus, the volatilization loss rate of 10%/yr
seems a reasonable estimate and corresponds to 114 kkg of the
1136 kkg of lead used in galvanizing in 1976. Disposal of lead-
galvanized products is taken at 25% (which includes the lead losses
due to the galvanizing processes, e.g., through dripping and spillage).
Losses to waters and POTWs are considered negligible because of the
relatively small amount of lead used in annealing and because of its
low solubility in water.
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26. Losses of lead due to the manufacture and use of lead foil are "
primarily to land, as a result of the disposal of lead foil wrapped
hazardous materials as well as foil trimmings. An estimated air- I
borne loss rate of 0.1% due to the rolling of lead into foil results •
in .an emission of 5 kkg from the 4649 kkg of lead used in foil.
The solid waste stream is taken to consist of about half of the •
foil produced, or 2324 kkg, because the foil is assumed to be used I
primarily for the packaging and disposal of hazardous waste. Lead
foil is also used to package radioactive materials in transit •
(U.S. Bureau of Mines I977a), and then it is discarded. A good I
portion of the foil is used to wrap low-level radioactive waste
that is then sent for storage/disposal. Lead loadings to water m
and POTWs are estimated to be zero because of both the small I
amount of lead used in foil and its low solubility in water. ™
27. The worldwide airborne emission factor for the combustion of fuel I
oils is, according to Nriagu (1978), 0.0091 kg/kkg. The amount of fuel •
oil burned in 1976 was about 289 million kkg (U.S. Bureau of Mines
1977a). Therefore, the airborne emission was 2630 kkg. Emissions •
to all other media as a result of oil combustion processes are I
assumed to be zero.
28. The combustion of coal, the production of iron and steel, and the •
smelting of copper and zinc result in substantial airborne emissions
of lead. Assuming a 75% emissions capture rate, then 75% of the «
captured lead can be assumed to be a solid waste, and the other I
25% remains an airborne emission. According to Nriagu (1978), the
worldwide emissions of lead from these processes are:
Coal combustion 14,900 kkg •
Iron and steel production 49,700 kkg
Copper and zinc smelting 42,300 kkg •
Coal used in the United States is about 15% of the worldxd.de value
(U.S. Bureau of Mines 1979); and only 85% of coal consumed in the •
United States is consumed as fuel (U.S. Bureau of Mines 1977b). |
Therefore, the U.S. emission of lead from coal combustion is:
(0.25) (0.85) (0.15) (14,900) = 475 kkg airborne emission I
And the corresponding solid waste emission resulting from airborne
emissions capture is: I
(0.75) (0.85) (0.15) (14,900) = 1425 kkg to land
For iron and steel production the United States uses 10% of the |
worldwide production or iron (U.S. Bureau of Mines 1978a). Assuming,
again, a 75% emissions capture efficiency overall, the airborne and •
solid emissions of lead due to iron and steel production are: I
Airborne: (0.10) (0.25) (49,700) = 1243 kkg —
Solid: (0.10) (0.75) (49,700) = 3729 kkg I
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Copper and zinc production are actually handled separately by
Nriagu (1978). Worldwide emissions of lead from copper production
and zinc production are 26,600 kkg and 15,700 kkg, respectively.
The corresponding portions of the worldwide use of copper and zinc
with the U.S. use in 1976 were 22.4% (U.S. Bureau of Mines 1975)
and 7.5% (U.S. Bureau of Mines 1978b), respectively. Therefore,
the corresponding U.S. emission would have been in 1976:
Copper production: 6000 kkg
Zinc production: 1200 kkg
Total 7200 kkg
Of the total airborne emission of 7200 kkg, the portion that is
assumed to be captured in emissions-capture devices is 75%, which
is assumed to be a solid waste. Therefore, the total lead emission
to land and air from the production of copper and zinc is:
Air: (0.25) (7200) = 1800 kkg
Land: (0.75) (7200) = 5400 kkg
29. These data are derived from the U.S. EPA MDSD's TABS DATA SYSTEM
and only includes data points that are currently in the database.
Consequently, these data are documentable, however, they represent
a minimum estimate of source discharges.
30. No data are available on the airborne lead emissions from the
refining of petroleum; however, it is possibly significant because
the amount of petroleum refined is very large.
31. Airborne and solid waste lead emissions from the mining of coal
are unknown, but probably small.
32. According to the SRI (1979) report on the agricultural sources of
lead, 95 kkg of lead are contained as an impurity in phosphate
fertilizers. The entire burden is assumed to be applied to land,
but no doubt a portion of runoff exists.
33. The estimate of lead discharges can be made based on preliminary
effluent data compiled by Burns and Roe (U.S. EPA 1980) and (U.S.
EPA 1977). The usefulness of such an estimate is only speculative
at best because data are available on 9 POTWs and effluent concen-
trations of lead are variable (0-53 yg/1). Removal efficiencies
for lead in POTWs also vary, although they seem to depend, to some
degree, on the influent concentration. According to the U.S. EPA
(1977), the national POTW flow rate is 22674.694 MGD. Based on 9
plants for which data are available, the average effluent concen-
tration is 19 yg/1 (U.S. EPA 1980). This is a mathematical average,
not a flow-weighted average.
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Annual discharge = (22674.694 x 106 ££i) (3 785 —
day ' gal
(19 x 10-9 ffls (365 days)
- 5.48 x 106 gms
=5.5 kkg
Accordint to SRI (1979), sewage sludge contains between 15 and 1900
mg/kg of lead. The amount of sewage sludge generated in 1976 was
3.6 million kkg. The distribution of sewage sludge is as follows-
254 is distributed to land as fertilizer; 25% is landfiLled- 15%
is ocean dumped; and 35% is incincerated. If the lead contained
in the sewage sludge that is incinerated is assumed to be half
volatilized and the other half stays with the ash and is landfilled
then the distribution of lead follows this pattern:
Air: 64 - 955 kkg
Land: 264 - 3683 kkg
Loses to water as a result of runoff are unknown.
34. These data are based on information on one plant; the information
was supplied by the U.S. EPA (1979). The identity of the plant
is unknown. It is assumed that this data point is representative
of all the plants and that all plants discharge directly.
35. According to the U.S. EPA (1975, 1976), approximately 200 domestic
plants manufacture lead acid storage batteries and battery oxides.
Recycling is highly prevalent among these plants. Virtually all
off-spec product is processed as well as most of the process wastes
and expended consumer materials. Approximately 32-114 kg of lead
containing waste solids are process derived per kkg of product
(U.S. EPA 1976). Approximately 0.015-0.61 kg of lead/kkg of pro-
duct occur as waterborne waste (U.S. EPA 1976). Based on 1972
production of 889,000 kkg the wastewater discharge of lead from
this industry is between 13 to 542 kkg. However, over 80% of the
lead subcategory plants discharge to POTWs (U.S. EPA 1976). Assuming
this ratio is reflected in the wastewater flow, 3-108 kkg lead are
discharged directly, and 10-434 kkg are discharged to POTWs. Only
about 30 kkg of wastewater treatment sludges are reported to be
disposed of annually. Presumably the remainder is recycled at the
plant and at a lead smelter (Versar 1980). Thus, it is expected
that land-disposed lead resulting from battery manufacture is
insignificant.
36. No data were available to estimate the losses to water, POTW or
solid waste from the production and use of lead as a gasoline
antiknock additive. However, these releases are expected to be
small relative to the airborne releases from this source.
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37. More than 90% of the lead content of ores is retained during
beneficiation (U.S. Bureau of Mines 1977a). Assuming that the
amount retained is 90%, then the total quantity of lead contained
in the ore from which the domestic supply of 517,897 kkg is
recovered is:
» 89 7 c-rr / /i 11
— = 575,441 kkg
Thus, the solid waste generated is the amount of lead that remains
in the ore tailings, which is the above amount, 575,441 kkg, less
the amount of lead recovered, 517,897 kkg, less the airborne
emissions, 1403 kkg, less the aquatic emission, which is 175 kkg
for both domestic and imported ore smelting and refining; this
latter amount, 175 kkg, can be proportioned between the imported
and the domestic amounts of lead recovered such that the aquatic
emission due to the production of lead from domestic ore is on the
order of 152 kkg. Thus, the total solid emission from the production
of domestic lead is:
575,441 - 517,897 - 1,403 - 152 = 55,989 kkg
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REFERENCES '
I
Hepple, P. ed. Lead in the environment. Essex, England: Applied
Science Publishers, Ltd.; 1971. •
Kirk-Othmer. Encyclopedia of chemical technology. Vol. 12. New York
NY: Interscience Publications; 1967. ' •
Lead Industries Association, Inc. U.S. lead industry 1977 annual review.
New York, NY: Lead Industries Association, Inc.; 1978. _
Nriagu, J.O. The biochemistry of lead in the environment. Part A. "
Amsterdam: Elsevier; 1978.
Sittig, M. ed. Environmental sources and emissions handbook. Park •
Ridge, NJ: Noyes Data Corp.; 1975.
Stanford Research International (SRI). Agricultural sources of lead. I
Contract No. 68-01-3867. Washington, DC: U.S. Environmental Protection
Agency; 1979. .
U.S. Bureau of Mines. Mineral facts and problems ~ copper. Washington,
DC: Bureau of Mines, U.S. Department of the Interior; 1975. _
U.S. Bureau of Mines. Mineral commodity profiles. Washington, DC:
Bureau of Mines, U.S. Department of the Interior; 1977a.
U.S. Bureau of Mines. Minerals yearbook metals. Vol. 1, minerals and •
fuels. Washington, DC: Bureau of Mines, U.S. Department of the Interior;
1977b. •
U.S. Bureau of Mines. Mineral commodity profiles, iron ores. Washington,
DC: Bureau of Mines, U.S. Department of the Interior; 1978a. •
U.S. Bureau of Mines. Mineral commodity profiles. Washington, DC:
Bureau of Mines, U.S. Department of the Interior; 1978b. »
U.S. Bureau of Mines. Commodity data summaries. Contract No. 68-01-3867.
Washington, DC: Bureau of Mines, U.S. Department of the Interior; 1979.
U.S. Environmental Protection Agency (U.S. EPA). Background information •
for new source performance standards, primary copper, zinc, and lead
smelters. Vol. 1: Proposed standards. Report No. EPA-440/2-74-002a. •
Washington, DC: U.S. Environmental Protection Agency; 1974. I
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U.S. Environmental Protection Agency; 1975.
" men^ SflS^'fVT*"1011 AgenC7 (U'S- EPA)- ^aft-development docu-
sta^dfrl1SUrh ^mitat10^ Sidelines and proposed new source performance
IanTS^fcal «™3 f*8* *** ^^ batteries se^nt of the machine rv
and mechanical products point source category. Washington DC- U S "
Environmental Protection Agency; 1976. n"ieconf UL. L.S.
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•
Washi"Stm' DC: ^-S- Environmental Protection
^^n Production and us* °f cadmium. Contract No. 68-01-385?
on, DC: U.S. Environmental Protection Agency; 1980
U.S. Environmental Protection Agency; 1979.
• POW ^i™"611"! ^ection Agency (U.S. EPA). Prelircinarv data for
E^roLtiai Prot-^ri^y^rGuidellnes Division'- E-S-
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U.S. Environmental Protection Agency |
Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Flow •
Chicago, IL 60604-3590 J
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