ENVIRONMENTAL LEAD
AND PUBLIC HEALTH
U. S. ENVIRONMENTAL PROTECTION AGENCY
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AP90
ENVIRONMENTAL LEAD
AND
PUBLIC HEALTH
R.E. Engel, D.I. Hammer, R.J.M. Horton,
N.M. Lane, L. A. Plumlee
ENVIRONMENTAL PROTECTION AGENCY
Air Pollution Control Office
Research Triangle Park, N. C.
March 1971
For sale by the Superintendent of Documents, U.S. Government Printing Office
Washington, D.C., 20402 - Price 26 cents
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The AP series of reports is issued by the Air Pollution Control Office to
report the results of scientific and engineering studies, and information of
general interest in the field of air pollution. Information reported in this
series includes coverage of APCO intramural activities and of cooperative
studies conducted in conjunction with state and local agencies, research
institutes, and industrial organizations. Copies of AP reports are available
free of charge to APCO staff members, current contractors and grantees, and
non-profit organizations — as supplies permit — from the Office of Technical
Information and Publications, Air Pollution Control Office, Environmental
Protection Agency, Research Triangle Park, North Carolina 27709.
Cover: The symbol on the cover was used by 18th century alchemists to
indicate lead, according to Bergman's alchemy table, dated 1783.
Air Pollution Control Office Publication No AP- 90
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FOREWORD
Environmental Lead and Public Health, a summary of the major public
health problems associated with lead, was written for a broader group of
readers than the professional scientific community alone. For those who
wish more detailed information than that provided in this report, appropriate
references to the literature are provided.
For each problem, the report succinctly discusses the scope and nature
of the problem; the present scientific and technological knowledge relevant
to its solution; the significant gaps in this state of knowledge; the predictions
on the growth of the problem; and, in some cases, alternative approaches to
its solution.
Several other reports on lead are being published by the Federal Govern-
ment. A technical state-of-the-art report on lead is being prepared for APCO
by the National Academy of Sciences. An interim report, Implications of
Lead Removal from Automotive Fuels: Interim Report of Commerce Tech-
nical Advisory Board Panel on Automotive Fuels and Air Pollution, pub-
lished in June 1970 by the U. S. Department of Commerce, outlines a
phased plan for removal of lead from gasoline. The final report is scheduled
for publication in 1971. Community guidelines for eliminating the problem
of lead poisoning among children in older urban areas will be detailed in
Control of Lead Poisoning in Children to be published by the Bureau of
Community and Environmental Management in 1971.
The interdisciplinary nature of the lead problem required the coopera-
tive efforts of many services within the U. S. Department of Health, Edu-
cation, and Welfare (DHEW) in the preparation of this report. The scientific
staff within the Air Pollution Control Office, in particular, Drs. Ronald E.
Engel, Robert A. Horton, and Douglas I. Hammer were responsible for ob-
taining and integrating the material presented in this document. Coordination
in the Environmental Protection Agency (EPA) was handled by Dr. Law-
rence A. Plumlee. Individual contributions were prepared by Public Health
Service Drs. Barry King, Herbert Stokinger, Harold Wolf, Jane Lin-Fu, Gran-
ville Lipscomb, and Mr. George Morgan. Additional contributions via
telephone came from Drs. Benjamin Pringle, Frances Marzulli, Dale Lindsay,
and Miss Helen M. Reynolds.
The EPA Lead Liaison Committee, the DHEW Intra-Departmental Com-
mittee on Lead Poisoning in Children, and the National Clearing House for
Smoking and Health provided guidance and review in the initial stages of
preparation.
ill
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The assistance of all the persons in EPA, Health Services and Mental
Health Administration, Food and Drug Administration, and other govern-
ment and private agencies who have made this document possible despite
many other pressing demands is most gratefully acknowledged. We hope that
all who read this report will find it a useful guide.
John T. Middleton
Acting Commissioner
Air Pollution Control Office
U. S. Environmental Protection Agency
IV
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CONTENTS
Introduction 1
Lead Metabolism and Toxicology in Man 3
Introduction 3
Absorption 3
Intoxication 4
Areas for Research 4
Lead in Diet and Consumer Goods 7
Introduction 7
Natural Sources 7
Drinking Water 8
Manufactured Sources 9
Current Status 10
Lead in Air 13
Introduction 13
Distribution of Ambient Lead Particles 13
Relationship of Particle Size to
Deposition in Human Lung 13
Sources of Atmospheric Lead 14
Methods for Measuring Atmospheric Lead 16
Atmospheric Surveillance 18
Current Status 19
Lead in Occupational Exposures 21
Introduction 21
Small Shops 21
Reporting and Diagnosis of Poisoning 22
Current Status 23
Lead Poisoning in Children 25
Introduction 25
Extent of Problem 25
Proposed Community Control Program 27
Economic Considerations 28
Current Status 28
References 31
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ENVIRONMENTAL LEAD
AND
PUBLIC HEALTH
INTRODUCTION
Elements that comprise less than 0.01 percent of an organism are com-
monly called trace elements. Some of these elements, such as copper, iron,
and zinc, are known to be essential for optimal biological function. Others,
such as cadmium, lead, and mercury, are not presently known to be neces-
sary for normal growth and metabolism. Large amounts of either essential or
nonessential trace elements may be toxic, however.
Natural lead deposits are ubiquitous; man nas been aware of the uses
and hazards of lead since the time of the ancient Greeks.1 In its natural
state lead has never been a major source of poisoning. The common forms of
lead poisoning result from the mining, processing, and commercial dissemina-
tion of the metal. Because as a metal it has several desirable properties such
as relative ease of refining from natural ores, malleability, and resistance to
corrosion, lead is used extensively in industry and in consumer goods. Indus-
trialization and urbanization have caused ecologic shifts resulting in increased
general population exposures to lead from man-made sources. Any health
effects caused by the increased lead exposures appear to be subtle, since
they do not cause any apparent clinical lead poisoning. Although lead poi-
soning does occur in animals,2'3 further discussion in this report is confined
to human effects.
Because lead is a known poison, it is necessary to identify and control
those conditions that result in excessive human exposure. For the same
reason, it is important to learn man's tolerance by determining what level of
intake causes the earliest signs of intoxication so that the appropriate mar-
gins of safety can be developed. To fully understand the effects of lead, one
must consider both its role in human physiology and its sources.
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The purpose of this document is to briefly summarize the major public
health problems associated with lead in the environment and the role that
the Department of Health, Education, and Welfare and EPA fulfill with
respect to these problems. Following a basic discussion of lead metabolism
and toxicology, the sections on diet and consumer goods and on ambient air
deal primarily with general population exposures. Because industrial workers
and children constitute two distinct exposure groups, they are discussed in
separate sections.
ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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LEAD METABOLISM AND
TOXICOLOGY IN MAN
INTRODUCTION
The chemical form of lead is an important determinant of its biological
behavior. Except in contaminated water, lead is rarely encountered in the
ionic form. Alkyl lead compounds, used primarily as automotive-fuel addi-
tives, are readily absorbed by skin and mucous membranes and are preferen-
tially distributed to the lipid phases of the body, including the brain. Such
properties make this organic form highly toxic, though in a different way
from inorganic forms.2 Since virtually all alkyl lead fuel is normally de-
stroyed during combustion, organic lead poisoning is a special problem
limited to a small group of occupational^ exposed workers. Further mention
of lead in this document refers to the inorganic forms, unless otherwise
specified.
ABSORPTION
Lead is primarily absorbed through the gastrointestinal and respiratory
tracts. Not all ingested or inhaled lead is absorbed or retained in the body,
however. The quantities of lead absorbed into the human body may be
estimated with fair accuracy from experimental evidence, which shows (1)
that somewhat less than 10 percent of the lead ingested daily under ordinary
circumstances is absorbed from the gastrointestinal tract and (2) that from
25 to 50 percent of the inhaled lead, dependent upon the size, shape, and
density of the particles inhaled, is retained and absorbed in the respiratory
system. The average quantity absorbed daily in the gastrointestinal tract of
the adult is of the order of 30 micrograms, and a reasonable estimate of that
absorbed in the respiratory system would be less than 20 micrograms for
urban dwellers.4- 5> 6 In the United States, lead intake in food and beverages
ranges from 100 to 2000 micrograms per day for an individual, with long-
term averages of 120 to 350 micrograms per day.
As lead intake is increased, the amount of lead retained also increases.
Clinical lead poisoning becomes apparent when the tolerance level is ex-
ceeded. In a series of careful feeding experiments, Kehoe showed that a
healthy adult man could eat 1 milligram of lead chloride per day for several
years without apparent ill health even though his body pool and blood lead
were increasing. In contrast, a subject eating 3 milligrams of lead chloride
per day developed signs and symptoms of clinical lead poisoning within 8
weeks.5 Lead retention is relatively poor, and prolonged exposure is required
for development of clinical symptoms of lead poisoning.
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INTOXICATION
Although all organs contain some lead, about 90 percent of the body
pool is found in the skeleton. The total body pool for a 70-kilogram man is
estimated between 100 and 400 milligrams.7 In practice, it is often necessary
to use the lead level in a readily accessible tissue, such as blood, as an index
of the body pool. Sometimes urinary lead is also used because specimens are
easy to obtain, but urine levels vary more than blood levels under similar
conditions.
Individuals with low levels of exposure have between 10 and 30 micro-
grams per 100 grams of blood; highly exposed individuals frequently have
blood-lead levels over 100 micrograms per 100 grams. Only persons exposed
to concentrated sources of lead are likely to have such high levels.
Clinical lead poisoning, or plumbism, is commonly characterized by
severe abdominal cramps, headaches, constipation, loss of appetite, fatigue,
anemia, motor-nerve paralysis, and encephalopathy. Almost exclusively con-
fined to children, lead-induced encephalopathy often leaves permanent brain
damage after both exposure and acute illness have ceased. To date, no cases
of plumbism have been reported in adults with blood-lead levels below 80
micrograms per 100 grams or in children with blood-lead levels below 50
micrograms per 100 grams.8
Clinical lead poisoning should be apparent to the physician. Such a
condition should have a subclinical stage wherein some early signs of distur-
bance are found by appropriate tests. Unfortunately, published reports of
clinical lead poisoning are still much more extensive than those on the early
subclinical or subtle changes.
Lead causes damage to the blood-forming system by altering both
hemoglobin synthesis and red-blood-cell-survival time. Although clinical
anemia has not been detected at blood levels under 50 and 80 micrograms
per 100 grams, in children and adults, respectively, recent work on hemo-
globin formation and red-cell survival indicates that early signs of disturbance
can be detected below this level in adults, but not in children.1'7 Examina-
tion of plasma delta-aminolevulinic acid levels [6-ALA] may eventually
prove useful as an indicator of lead toxicity.9' 1 °> 11 Plasma delta-amino-
levulinic acid dehydrase (6-ALADH) also seems to be a sensitive indicator of
blood lead. The activity of this enzyme correlates negatively with blood-lead
levels ranging from 5 to 95 micrograms of lead per 100 grams of blood.12
AREAS FOR RESEARCH
In contrast to the considerable amount of research directed toward
detection of subclinical lead poisoning, there has been little investigation of
early and late effects on organ systems other than blood, such as bone,
ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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kidney, liver, and the nervous system.13 16 Blood-lead levels do not accu-
rately reflect the body lead pool and may not be the optimal measures of
exposure in the general population. Knowledge of the factors that favor the
release of lead from body storage sites is essential for determining the con-
tribution of the various lead sources to the total environmental hazard. Also
necessary is the estimation of the total body burden that can be tolerated
considering possible shifts of body stores.
Other gaps in the knowledge of the etiology of lead poisoning fall into
three main categories. The first is the lack of information regarding possible
long-term, or chronic effects of lead at environmental levels of exposure,
especially at levels that do not produce apparent clinical lead poisoning.
Although it is known that lead accumulates with age in the skeleton, kid-
neys, liver, aorta, pancreas, and lungs, few follow-up studies have been made
on the present health status of people exposed to excessive lead levels 20 to
50 years ago.6 The few reported studies are contradictory.
The second gap is the paucity of information on the effects of exposure
on groups of individuals in the general population who might be especially
sensitive to lead. This sensitivity might be permanent or temporary. Meta-
bolic abnormality such as glucose-6-phosphate dehydrogenase (G6PD) defi-
ciency and sickle cell disease are examples of permanently altered sensitivity.
Temporary increased sensitivity may be associated with a particular age
period of growth, of pregnancy, or of illness. Particular attention should be
directed toward elucidation of the mechanisms by which lead produces the
central-nervous-system syndrome in children and not in adults. The possi-
bility that lead exposure from conception could enhance the onset or
severity of disease should be explored. Emphasis should be placed on
determining whether the fetus of a mother exposed to elevated environ-
mental concentrations of lead is even more sensitive to lead encephalopathy
than the 2-year-old child.
The third gap in our knowledge is that little scientific information on
the possible effects of interaction of lead with other environmental chemicals
is known. The chemical diversity and complexity of our environment neces-
sitates the study of such interactions.
Although blood and urine are commonly used to determine clinical
illness and increased exposure, additional indices more closely related to the
total body-lead pool are needed to evaluate low-level exposures. The use of
hair and teeth, which are easily accessible tissues, has been recommended,
and a few pilot studies have indicated their potential usefulness.13' 17>18
More detailed studies are needed.
Improved methods of treatment should reduce, not only the number of
deaths, but also the residual effects in survivors. Studies of children who
have elevated body-lead levels and who appear clinically asymptomatic would
help to determine the subtle effects of lead poisoning that are not immedi-
ately apparent. Such studies could provide biomedical tools for determining
Lead Metabolism and Toxicology in Man
-------
the effectiveness of treatment, and for detecting and preventing high body
burdens of lead.
ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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LEAD IN DIET AND CONSUMER GOODS
INTRODUCTION
The diet is the principal source of lead uptake among the general popu-
lation. All natural foods contain small quantities of lead, the level varying
according to their growing environment. There is no food source known,
however, to concentrate lead selectively from the soil. This is in distinction
to other trace elements, such as copper and selenium.
Since lead is widely used in equipment and containers involved in food
processing, prepared foods and beverages may become contaminated. Histori-
cally, direct contamination of food and drink has been the major source of
lead poisoning among general populations. Acidic foods, in particular, can
leach lead from cooking, serving, and storage utensils made from metal
alloys, or from pottery improperly glazed with lead compounds. It has re-
cently been suggested that the widespread use of lead in the cooking utensils
of the Roman upper classes contributed to the fall of Rome.19
NATURAL SOURCES
Fruits and Vegetables
Past concern with lead arsenate used as a pesticide on fruits and vege-
tables resulted in establishment of Federal Tolerance Limits for lead arsenate
residues on selected agricultural raw products. Except for citrus fruits, whose
acidity requires a limit of 1 part per million (ppm), the limit is 7 ppm where
the regulation applies.20 Since 1945 the use of lead arsenate has been de-
clining, but over 5 million pounds was still used on fruit* and tobacco in
1968.21 Moreover, soils in some areas still have evidence of heavy contami-
nation with the stable lead arsenate compound.22 Preliminary evidence from
limited studies of crops growing near highways suggests that, other things
being equal, plant residues and uptake decrease exponentially with the dis-
tance from the highway.23
Lead in milk poses no current threat to public health even in areas with
pollution problems.24
In a recent study of dietary trace metals the total lead content found in
sample American diets was approximately 0.03 microgram per gram. The
*Seventy percent of the 5 million pounds was used in apple orchards.
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lead levels in individual foods varied from 0.08 to 0.3 microgram per gram in
some local market products.25 Certain foods consistently contain more lead
than others.26 The assay techniques have not yet been adapted to include
lead among the pesticide residues routinely monitored in the U. S. Food and
Drug Administration's Market Basket Survey of dietary components.
Fish
Bacterial decomposition of organic matter is inhibited by lead concentra-
tions in water equal to or greater than 0.1 milligram per liter.27 As with
many other elements, lead is more toxic to fish in soft water than in hard
water.28 Little is known about the ability of fish, other than shellfish, to
concentrate lead in their edible portions, but levels found by limited surveys
of marketed oysters and clams were not considered dangerous for human
consumption.29"32 Since oysters can concentrate up to 328 ppm lead from
0.2 ppm lead in sea water after 10 weeks exposure in a controlled environ-
ment, it can be assumed that oysters living in waters with a high-lead con-
tent will have high concentrations of lead in their edible portions.30 If
environmental pollution at the shellfish resources is allowed to continue
unheeded, levels in such food could present a serious public health problem
in the very near future.
DRINKING WATER
Water Supplies
Drinking water supplies have been monitored for lead by the Water
Pollution Surveillance System since 1962, and the lead content has not gen-
erally exceeded the prescribed standard of 0.05 milligram per liter of wa-
ter.28 In one recent 5-year summary of trace metals in rivers and lakes of
the United States, sponsored by the Federal Water Pollution Control Admin-
istration, the maximum recorded lead concentration was 0.140 milligram per
liter, with about 2 percent (27/1700) of the samples containing lead in
excess of the limit.33 The sample locations that had the higher levels could
usually be related to metal working industries situated along a river. Data
from the Bureau of Water Hygiene of the Environmental Control Adminis-
tration, collected from each of the nine Public Health Service regions across
the country, showed that only 2 percent of the drinking water samples
exceeded the PHS limit in 1969, but over 75 percent of the samples ana-
lyzed by atomic absorption specrometry had detectable lead levels.34 Some
of the elevated lead levels in the tap water samples can probably be attrib-
uted to lead pipes.
Most samples for such monitoring surveys are taken from or near water
plants. More extensive surveillance of consumer tap samples would be desir-
able, and would provide more assurance that the level of lead in drinking
water was truly reflecting the compliance with the standards.
8 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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Water Pipes
There have been serious outbreaks of lead poisoning in Europe, where
lead pipe has been commonly used in exterior and interior plumbing. Most
of these outbreaks, however, occurred many years ago. In this country, iron,
galvanized, and copper pipes are used; however, the use of lead pipe is still
permitted by many plumbing codes. Some lead is also used at the joints in
caulking or soldering, but not in quantities to cause any hazard. The use of
lead pipes is generally harmless with most water supplies, but some waters
dissolve lead from plumbing. The reasons for this are not all known, but
naturally soft waters, which are slightly acid and low in mineral content, are
the most corrosive.35
MANUFACTURED SOURCES
Ceramic Glazes
Recently, the Food and Drug Administration (FDA) has been concerned
with the lead in ceramic glazes, inserts on tableware, and pottery serving
dishes. Most of the items inspected have been of foreign, rather than do-
mestic, origin. In fact, the recent episodes of lead poisoning from glazes on
imported pottery initiated an FDA study of all suspect foreign ceramic pro-
ducts. Having found several import items in that category, the FDA has
designed a parallel study of domestic dinnerware, to be completed in the
near future.
In one study of random market samples, pottery with glazes in cones
three to five times the temperature at which most commercial domestic
dinnerware is fired, released only 0.02 to 0.45 microgram of lead per milli-
liter of leaching solution.36 That test, however, was based on a 30-minute
exposure to a hot (60° C) leaching solution.37 Experience in FDA labora-
tories has shown that length of exposure is a critical factor in determining
the amount of lead released.38
As of July 1970, the working action level with respect to extractable
lead in clear ceramic glazes was 7 micrograms per milliliter, released after
soaking the piece for 24 hours at room temperature in 4 percent acetic acid.
The Division of Compliance in the Bureau of Foods, FDA, now attempts to
remove from the market any dinnerware that releases more lead than al-
lowed by this interim standard.
Moonshine
Historically famous episodes of lead poisoning from direct contamina-
tion of alcoholic beverages have been attributed to lead cooling coils in rum
stills (West Indies Dry Gripes), lead linings and joints in cider presses (Devon-
shire Colic), and lead compounds used for cleaning and preserving wine
(Poitou Colic). Although none of these situations now exist in licensed alco-
holic beverage industries, illegal whisky production in some areas of this
Lead in Diet and Consumer Goods
-------
country is still a cause of lead poisoning. In 1969, thirty percent of the
moonshine whiskey samples taken by the Atlanta regional office of the
Treasury Bureau's Alcohol and Tobacco Tax Unit contained more than 1
milligram of lead per liter.39 Most of these stills are made from old
lead-coated automobile radiators with lead solder connections. There is some
evidence that "moonshine" lead is the cause of sterility, spontaneous abor-
tion, and neonatal malformation among steady female consumers.40
Color Additives and Hair Dyes
Some foods, cosmetics, and drugs contain lead in color additives. The
Food and Drug Administration currently permits this use of lead at a
working limit of 10 ppm in food and 20 ppm in drugs and cosmetics.20
In a number of men's hair coloring preparations on the market the
principal active ingredient is lead acetate; the average lead concentration is
about 2 percent.41 As of July 1970, lead acetate was neither provisionally
nor permanently listed as an official color additive by the Food and Drug
Administration. There is no current official objection to the use of lead
acetate in hair dyes provided the labels bear cautionary statements against
use on cut or abraded scalps, and a warning to wash hands throughly after
use.
On the basis of animal and human studies with lead acetate hair dyes
the industries have issued a preliminary report stating that the hazard of lead
absorption among the users is negligible. FDA toxicologists are still evalu-
ating the industrial report.42 Meanwhile, the Dermal Toxicity Branch is con-
ducting studies to determine the degree of dermal absorption.
Cigarettes
Like most plants, tobacco contains some lead. Although most tobacco
lead remains in the ash, a little less than 1 microgram is present in the
smoke of one cigarette.
Examination of blood lead levels in smokers and nonsmokers has pro-
duced differing results.43' 44 The disparity may have been due to difference
in lead analysis techniques. Even so, average blood-lead levels in all subjects
in all studies have been well within the normal range. It is still possible,
however, that cigarette smoking may contribute to an increased body burden
of lead since higher mean lead concentrations have been found in the cal-
varium, rib, and lungs of smokers than in nonsmokers.44
CURRENT STATUS
The Federal Government maintains a limited program of surveillance for
lead in consumer goods primarily based on isolated incidents of poisoning
10 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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due to excessive contamination. Regulations are, therefore, set for specific
items, but not based on total dietary consumption. There is at present no
standarized monitoring system, nor a standardized lead assay technique for
mass sampling although both are on the FDA's list of planned projects and
on-going research.
Drinking water supplies are monitored by the Water Quality Office of
the Environmental Protection Agency and certified only when their lead
content is less than 0.05 milligram per liter. The major drawback in the
system is the fact that the water taps themselves are not usually monitored.
Tap water monitoring would assure the consumer that the water lead level
actually reaching him was no greater than 0.05 milligram per liter and would
act as a monitoring system for the delivery network.
Although little is known about the degree to which fish concentrate lead
in the edible portions, lead is known to concentrate in oysters. It is, there-
fore, reasonable to conclude that oysters living in a water environment high
in lead could constitute a public health hazard if marketed and consumed.
Illegal moonshine whiskey made in stills using automobile radiators as
condensers is the principal recognized source of excess lead in dietary con-
sumer products. This source of lead comsumption is being reduced through
increased public education and through full enforcement of regulations ban-
ning illegally distilled whiskey.
The cosmetics industries, the U. S. Pottery Association, and the Inter-
nationa] Lead-Zinc Research Organization in cooperation with the FDA are
studying the physiologic, pharmacologic, and toxicologic effects of lead com-
pounds in both ingestion and topical exposures encountered in consumer
products.
Lead in Diet and Consumer Goods 11
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LEAD IN AIR
INTRODUCTION
Most airborne lead is associated with particles ranging between 0.1 and
5.0 microns in diameter, with a mean for urban air of 0.25 micron.45'46
Particle size distribution is an important consideration since it determines
both the amount and the nature of airborne contamination. Although larger
and heavier particles settle out within a short distance from the source,
smaller particles remain airborne and may be carried great distances de-
pending on meteorological conditions. Size and shape also determine the
deposition, retention, and absorption of lead particles in the human lung.
DISTRIBUTION OF AMBIENT LEAD PARTICLES
Data on the size distribution of particulate lead indicate that most of
the ambient lead particles are less than a micron in diameter. A study at
Berkeley, California, showed that 50 to 80 percent of atmospheric lead
occurred in particles of less than 1 micron in diameter; in Los Angeles 90
percent of the atmospheric lead was found in particles smaller than 1.6
microns in diameter.47
Particulate lead in urban Cincinnati had an average mass median dia-
meter (MMD) in the 0.18- to 0.30-micron range, whereas an average MMD of
0.74 micron was found at a remote site 40 miles from Cincinnati.45 The
average MMD of lead particles in such "background" air had a large variance.
An average MMD similar to those in urban areas indicated "young" back-
ground particles, those that were transported or dispersed to the site by
rather high-velocity winds. A relatively high average MMD, like the 0.74-mic-
ron example, indicates "old" particles, which probably resulted from mid-
transit coagulation.48 The average MMD of particulate lead ranged from 0.23
to 0.31 micron in samples collected by means of the Goetz aerosol spectro-
meter in Chicago, Cincinnati, Philadelphia, Los Angeles, Pasadena, Vernon,
San Francisco, Cherokee, and Mojave in 1963.46
RELATIONSHIP OF PARTICLE SIZE
TO DEPOSITION IN HUMAN LUNG
When airborne particles are inhaled, they may be deposited on the mu-
cus membranes of the nose and throat or in the parenchyma of the lungs.
13
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About half of the inhaled particles reaching the lung are deposited; the rest
are exhaled. The quantity and location of the deposition depends principally
on the size and chemical composition of the particles.49 Particles over 5.0
microns in diameter are primarily deposited in the nose and throat. In gen-
eral, as the size of the particle decreases, the deeper the particle is deposited
in the respiratory tract.49
In the submicron size range, 36 to 51 percent of experimentally inhaled
particles were deposited from an experimental dose of 150 micrograms of
lead acetate per cubic meter of air. Following these exposures, an increase in
detectable blood lead with little, if any, increase in fecal lead50 indicates
that some retention and absorption of the smaller particles did occur.
Men chronically exposed to 10 micrograms per cubic meter of 0.05-mic-
ron-diameter lead particles showed inconclusive evidence of increased lead
absorption as measured by blood and fecal lead.51 Similar experiments using
20 micrograms per cubic meter have been completed, but results have not
been reported. Mice exposed for 15 months to low levels of nonirradiated
auto exhaust in a cyclic diurnal pattern contained more lead in their bones
than corresponding groups exposed to equal or slightly lower concentrations
of irradiated auto exhaust even though the daily average lead concentrations
were about the same in both atmospheres. Mice exposed to as little as 2.6
micrograms per cubic meter of lead in nonirradiated exhaust had bone lead
concentrations higher than control mice.52
SOURCES OF ATMOSPHERIC LEAD
Total estimated United States lead consumption increased 9.6 percent
(1,202,283 to 1,318,809 tons/year) from 1964 through 1968.53 Lead used
as gasoline antiknock additives increased an estimated 17.1 percent during
this same time period. These fuel additives represent a high potential atmo-
spheric lead source and accounted for 19.9 percent of 1968 consumption;
58.0 percent was probably recycled and 22.1 percent was insignificant with
respect to atmospheric pollution. In this same year lead from gasoline com-
bustion represented an estimated 96.4 percent (180,000 of 186,614 tons) of
lead emissions. Thus 68.7 percent (180,000 of 261,897 tons) of fuel ad-
ditives was emitted to the atmosphere as opposed to 0.6 percent (6,614 of
1,056,912 tons) of all other lead consumption. Not surprisingly, urban am-
bient lead levels ranged from 5 to 50 times higher than those of nonurban
areas.
Primary and Secondary Lead Smelters
About 980 tons of lead was emitted to the atmosphere from primary
14 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
-------
and secondary lead smelting operations during 1968, i.e., approximately 0.5
percent of the total lead emitted to the atmosphere. Whereas particulates of
metallurgical dust and fume cover a particle size range of roughly 0.001 to 100
microns, the fume has a particle size range from 0.01 to 2 microns.55'56
Concentrations of lead reaching several milligrams per cubic meter have been
observed at ground level downwind from smelters. The average lead content of
the earth's crust is 16 ppm, but values of several thousand parts per million
may be found near smelters. Because of these high air and soil levels, smelters
represent potential point-source public health problems in addition to their
known risk of occupational exposures.
Other Industries
Excluding gasoline antiknock additives, industrial uses have accounted
for approximately 85 percent of the total United States consumption. Emis-
sions from industrial sources other than primary and secondary lead smelters
account for approximately 2 percent of the total atmospheric emissions in
1968. In brass founding, for example, molten lead that is overheated during
production processes is emitted as lead fumes or particles, in the size range
of 0.01 to 2 microns in diameter.
The manufacturing of lead alkyl contributes approximately 810 tons of
lead per year to the atmosphere. Nationally this represents only 0.43 percent
of the total, but the emissions are concentrated and can present localized
health problems. Also in the event of an accident, high local concentrations
can occur. The transfer of gasoline from one container to another accounted
for release of 40 tons of lead in the air in 1968.
Combustion of Coal and Fuel Oil
Because coal and fuel oil contain lead, airborne particulates derived from
their combustion may also contain appreciable quantities of lead. Coal com-
bustion contributed approximately 920 tons of lead (0.5%) to the atmosphere
in 1968; fuel oil combustion contributed 24 tons (0.01%).54 Concentrations of
lead as high as 150 ppm in fly ash and 358 ppm in soot have been reported
near coal-burning electric power plants.46
Incineration
Burning of waste crankcase oil in 1968 produced 3,000 tons of lead
emissions, amounting to 1.6 percent of the total estimated emissions. Incin-
eration of solid wastes in municipal incinerators released 320 tons of lead to
the atmosphere in 1968-roughly one-third of fuel oil and coal combustion.
Like most other general sources of ambient air lead, other than automobile
exhaust, emissions on a national basis have probably been underestimated.
Lead in Air 15
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Automotive Exhaust
Production of gasoline antiknock additives represent about 20 percent of
the total lead used in the United States in 1968. In contrast, the exhaust
from gasoline-fueled vehicles accounted for approximately 97 percent of the
airborne lead. Nearly all engine gasolines sold in the United States contain
lead alkyl compounds added to improve the antiknock quality of fuels with-
out expensive additional refining. The maximum concentration of lead
permitted in gasoline is set at 4.2 grams per gallon, a value agreed upon by
the producers of gasoline and accepted by the Surgeon General of the
United States in 1965. Average concentrations of lead in gasoline have risen
from 2.32 grams per gallon in 1963 to 2.59 grams per gallon in 1970.57
Lead alkyl compounds are converted to lead halides and lead oxyhalo-
genates in the internal combustion engine, and 70 to 80 percent of that lead
is emitted as particulate matter from the tailpipe.46 The age and condition
of the vehicle as well as the design of the engine and exhaust system govern
the particle size and the amount of lead emitted to the atmosphere. About
95 percent of total lead in the particulate components in hot, concentrated
automobile exhaust and in cooled diluted exhaust was associated with
particles having aerodynamic diameters below 0.5 micron.58 The relatively
high concentration and submicron size of particulate lead in automobile
exhaust are consistent with atmospheric measurements.45' 46
Lead alkyl compound also reaches the atmosphere directly by evapora-
tion from gas tanks, from carburetor vents, and during filling at the service
station. Lead alkyl additives also interfere with catalytic exhaust treatment
systems designed to reduce hydrocarbon emissions. Principally because of
this, and not from health considerations alone, the Department of Com-
merce, Technical Advisory Board Panel on Automotive Fuels and Air Pollu-
tion, and the Department of Health, Education, and Welfare have recom-
mended that legislation be enacted to establish the authority of the Federal
Government to regulate the use of automotive fuel additives, requiring the
availability of low-lead fuel by 1972 and unleaded fuel by 1974.59 Tax
incentives on production of both of these fuels have been recommended by
some agencies because of the slightly higher cost of producing nonleaded
high-octane gasoline. The economic burden of producing an unleaded gas-
oline of the desired octane will fall heavily on small refiners.5 9
METHODS FOR MEASURING ATMOSPHERIC LEAD
Sample Collection
The most commonly used methods for collecting air particulates for lead
analysis involve filtration through either a glass fiber or membrane filter for
24 hours.60 Cellulose filters may be used, but they are not recommended
because of variation in collection efficiency. Particles collected by the filtra-
tion method fall in the 0.1-micron-diameter range; the usual practice is to
16 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
-------
sample for a 24-hour period. In order to determine lead content in the
larger, settleable particulates, samples are collected by means of a dustfall
procedure, usually over a period of 30 days.
Special sampling devices that can separate airborne particulates by size
are available if there is a need to determine the particle size distribution of
lead. These samplers are not in common use because of their high cost, low
sampling rate, and complexity of operation.
Organic lead—lead tetraethyl, and lead tetramethyl—can be trapped by
passing pre-filtered ambient air through an absorbing train containing crystal-
line iodine or high-purity activated carbon. Although the system is cumber-
some and time consuming, and requires constant attention, it performs
adequately for the collection of gaseous lead compounds in the microgram-
per-cubic-meter range.
Sample Analysis
By suitable processing, both the particulate and gaseous lead samples are
converted into solutions of lead salts that may be analyzed by any one of
several acceptable methods. Although lengthy and tedious, the colorimetric
Dithizone method, which has been the method of choice for a number of
years, is very specific, accurate, and precise.61 The use of atomic absorption
spectrometry has gained widespread acceptance within the past 5 years
because its high initial instrumentation cost is offset by its speed and ac-
curacy. Satisfactory results can be obtained by the use of emission spectro-
metry or polarographs, but these methods require a greater degree of analyti-
cal skill than atomic absorption spectrometry. An instrumental method that
would permit the direct, simultaneous measurement of gaseous and particu-
late atmospheric lead on a continuous basis is currently under development.
Air samplers currently available for sampling a variety of size ranges of
airborne particulates differ in their capabilities and sampling rates. A recently
developed air sampler, presently being field tested, promises to provide ade-
quate samples for determination of size distribution of lead particulates over
a wider range than is currently possible.61 At present the Air Pollution
Control Office (APCO) uses the Lee modification of Anderson Cascade im-
pactor* and electrostatic fractionator.
To fully assess this aspect of ambient air lead levels, the National Air
Surveillance Network (NASN) of APCO instituted a network early in 1970
to determine the size distribution of lead and other components in the air at
six major urban areas. Special short-term studies are being conducted to
gather additional data relative to particle size distribution and ambient levels
at selected sites.
*Use of a company or product name does not constitute endorsement by the U. S.
Environmental Protection Agency.
Lead in Air 17
-------
Limited studies of particle size distribution have been carried out in the
San Francisco Bay area. Ordinarily, two fractions are obtained with a cen-
trifugal separator, but Cascade Impactors are sometimes used to provide four
or more fractions. The Kettering Laboratory of the University of Cincinnati
College of Medicine conducts intermittent particle size distribution studies as
part of a long-term lead project. Short-term studies are frequently done in
the Los Angeles area by the University of California, Riverside, with the
Lundgren Impactor sampler. Stanford Research Institute uses the Goetz
Aerosol Spectrometer in special contract studies relating to atmospheric lead.
ATMOSPHERIC SURVEILLANCE
Routine Surveillance of Particulates
The National Air Surveillance Network operates about 270 glass-fiber
filter samplers for measuring airborne particulate pollutants in urban and
nonurban areas throughout the United States. Samples are collected over a
24-hour period every 2 weeks on a random schedule and analyzed for lead
and 35 other trace metals by emission spectrometry.62"66 National Air Sur-
veillance Network data through 1966 have been published, and more recent
data are scheduled for publication early in 1971. Many state and local air
pollution control agencies conduct particulate surveillance programs similar
to that of APCO. Some of the samples generated by these networks are
analyzed for lead, and the data are contributed to APCO's National Aero-
metric Data Bank.67
The combined Federal, State, and local effort provides reasonably ade-
quate definition of ambient lead concentrations for all cities over 50,000
population, for many with less than 50,000 population, and for a cross
section of nonurban areas. New York City also conducts special particulate
surveillance programs, which include measurement of lead.
Routine Surveillance of Organic Lead
There is presently no organized routine surveillance program for deter-
mining organic lead in ambient air. The current method for assaying lead in
samples of particulate pollutants does not distinguish between organic and
inorganic lead compounds. Organic lead is thought to contribute only trivial
amounts to total ambient air levels.
Urban Versus Nonurban
The effect of civilization on lead emission becomes obvious when con-
centrations at urban stations are compared with those at nonurban stations.
Average particulate lead concentrations at urban stations for 1965 ranged
quarterly from 0.1 microgram per cubic meter in Paradise Valley, Arizona,
to as much as 2.3 micrograms per cubic meter in Burbank, California.66 In
18 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
-------
contrast, the range of averages at nonurban stations was an order of magni-
tude lower than that at the urban sites. They ranged from no detectable
concentration at the White Pine County, Nevada, station to 0.17 microgram
per cubic meter at the Washington County, Rhode Island, station. Nonurban
stations may be perceptibly influenced by surrounding urban areas and/or
highway traffic. Even the "remote" stations are located in national park
areas, where electricity is available, and where there is tourist traffic during
at least some seasons. These remote stations may therefore owe some por-
tion of the lead detected there to man's activities.
Special Studies of Selected Cities
In 1961-1962, a 12-month study of ambient-air- and human-blood-lead
levels was made in Cincinnati, Los Angeles, and Philadelphia.68 Extensive
measurements of lead in the three cities showed variations with season of the
year and location in the city; these data were found to conform to the range
of urban concentrations reported by the national network.68 The highest
seasonal lead concentrations typically occur in the fall and winter. Ambient-
air lead concentrations are also a direct function of traffic density and speed.
Cholak and co-workers reported that the lead content of soil in the Cincin-
nati area varied from 16.4 to 360 ppm.69
A similar study in the same cities and four additional large cities-
Chicago, Houston, New York, and Washington— will be completed by the end
of 1971. In these studies, six to eight sampling stations are operated in each
city at sites selected to provide a reasonable lead profile for the city. For
each city, a nearby area with a minimum of lead sources is selected to
provide comparable information of suburban background lead levels, when
possible.
CURRENT STATUS
Lead air pollution problems still occur in areas near lead smelting and
reprocessing plants, lead-using industries, and coal-burning electric power
plants. Small amounts of airborne lead come from soils and from solid waste
incineration.
Although particulate sampling devices currently used by NASN to mea-
sure ambient pollutants do not have the capability of collecting total
atmospheric lead, various components of the Government and industry are
deeply involved in the development of an acceptable sampling device. Tech-
niques to provide accurate, economical, and rapid measurements of atmo-
spheric lead are also being developed.
Limited research has indicated that ambient lead concentrations are a
function of season, location, and traffic density and speed. More intensive
studies are being conducted to fully define the role of other pollutants and
Lead in Air 19
-------
variables in determining the lead concentrations in ambient air and relating
the levels to health effects.
Lead in automobile fuels is the major source of atmospheric lead.
Various committee studies, research and development, and other activities
continue to develop the Federal position relating to reduction of the atmo-
spheric lead levels contributed by the automobile.
20 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
-------
LEAD IN OCCUPATIONAL EXPOSURES
INTRODUCTION
Industry will probably remain a major source of excessive lead exposure
because of the wide use and versatility of the metal. Where most severe
exposures among the general populace have been due to lead ingestion, ex-
posures among industrial workers have been primarily due to lead inhalation
from fumes and dusts produced by heating, pulverizing, and grinding the
metal. Industrial hygiene measures for controlling workers' exposure have
been developed for nearly all recognized processes. Incidence of clinical lead
poisoning in the past has usually been attributed to unrecognized exposures
introduced with new industrial processes. The incidence, however, has de-
creased as knowledge of lead toxicity and hygienic technology has increased.
Efforts have been made to reduce exposure in many work categories below
the minimum acceptable limits through the enforcement of safe work stan-
dards for lead in air and urine set by the Walsh-Healy Act.70
In a 1964 U. S. summary of industrial exposure, measurements of lead
in inplant air and employee urine samples showed that since 1934, exposure
had decreased by several magnitudes for workers in seven of eight categories
representing the major uses of lead.71 The report did not note that over-
exposure to lead was common in small shops nor include data on munitions
plants.
To up-date this survey, the Bureau of Occupational Safety and Health
telephone-interviewed 24 key individuals across the country who were re-
sponsible for the control of industrial lead exposures. The 1969 survey indi-
cated that overexposure to lead still occurs: (1) in small shops, (2) among
itinerant workers (e.g., construction workers), and (3) where new or unusual
lead-using processes had been introduced. Repeated lead poisoning has oc-
curred, for example, in crews spraying lead-based paint to renovate missile
silos.72 Problems of inadequately staffed and supported occupational health
facilities noted in 1964 were also found unimproved in the 5-year period.
The survey found that improved control of lead exposures had resulted from
(1) removal of the source of exposure, for example, substituting titanium for
lead in paint or using construction materials not requiring lead paint; (2)
orientation of supervisors; (3) improvement of monitoring; and (4) improve-
ment of control techniques.
SMALL SHOPS
Small-shop operations, in particular battery recovery and welding, are
21
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responsible for the largest group of uncontrolled lead exposures. The types
of plants, operations, and sources that should be monitored for suspected
cases of lead exposure are legion. One state health department surveyed 23
small shops* from 1966 through 1969.73 About 20 percent (118 of 568) of
all blood samples drawn during these 4 years exceeded 80 micrograms of
lead per 100 grams of blood. Blood levels exceeding this limit were con-
sidered presumptive evidence of overexposure to lead since these workers
were not clinically examined by a health department physician. This same
health department was effective in preventing one company with a particu-
larly bad record of overexposures to lead from locating in its jurisdictional
area.
Another state set threshold limit values of 200 micrograms per cubic
meter of industrial air based on a 40-hour work-week exposure, but found
levels above this in 35 percent of 537 samples taken in 1967.74 Most of
these were also in small-shop operations.
Itinerant construction workers, though fewer in number, pose an even
more formidable problem for control agencies because the workers are
usually not available for regular checkup.
REPORTING AND DIAGNOSIS OF POISONING
Most industrial hygiene laboratories now use blood-lead levels in addi-
tion to air-lead levels to monitor and regulate worker exposures. Some use
stippled-cell counts; a few, urinary lead and/or coproporphyrins levels; fewer
use urinary delta-aminolevulenic acid (5-ALA) levels routinely; and none
routinely use blood 5-ALA dehydrase levels.12 Some laboratories sample
workers' blood either quarterly or annually; others sample when overexpo-
sures are suspected during and after surveys or on a demand basis. Quarterly
sampling is done when the surveys indicate a need for more information.
Medical examinations are performed in addition to the biological and en-
vironmental analyses when physicians are available.
Blood-lead levels are generally accepted as superior to urine levels as
indicators of lead intoxication. Nevertheless, industrial hygienists and phy-
sicians comparing medical reports with laboratory data have commonly
noted that many workers have blood-lead levels far in excess of recom-
mended limits, but show no signs or symptoms of lead intoxication. Hence
an elevated blood-lead level per se is not conclusive evidence of clinical lead
poisoning. The number of reported "mild, chronic" cases may therefore be
exaggerated because the diagnosis is usually based on blood levels alone.
Lead intoxication, particularly in its early stages, is difficult to diagnose.
*Battery manufacture and rebuilding, can manufacture, chemicals, communications, elec-
trical work, exterminating, food processing, glass manufacture, junk yards, newspaper
and print shops, machining, metal working, paint manufacture and application, fuel
blending, plastics, phonograph records, police rifle range, packaging, refrigerator man-
ufacture, ship salvage, smelting and refining, trucking, and vocational training.
22 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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The development of refresher courses in occupational medicine and the es-
tablishment of a nationwide compulsory reporting system for occupational
exposures would both help to identify and consequently reduce this prob-
lem.
Cases of acute lead poisoning are rarely reported in large industries with
well-staffed medical or industrial hygiene departments or in states and local
jurisdictions with well-staffed occupational health departments. Unfortu-
nately cases are rarely sought in areas with less well-staffed health depart-
ments and have even been found in certain branches of the U. S. Armed
Forces where widespread small operations are common. Inadequate investiga-
tions because of understaffed agencies, opening of new small shops, failure
to diagnose early lead poisoning, and problems in blood lead analysis have all
mitigated against improvement.
CURRENT STATUS
Industries with good occupational health departments have minimized
lead exposure problems. Nevertheless problems still occur in places with
inadequate control by reason of peculiar work situations, itinerant workers,
new operations, small shops, or inadequate medical laboratory and/or occu-
pational health services. There is still need for more uniformity and vigor in
the control of industrial lead exposures.
The problems of industrial lead exposure are being reduced by better
enforcement of present legislation, enacting new legislation where needed,
increasing the number of occupational health physicians and industrial hy-
gienists, establishing refresher courses for both industrial and non-industrial
physicians, and certifying medical laboratories for tissue lead analyses.
Lead in Occupational Exposures 23
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LEAD POISONING IN CHILDREN
INTRODUCTION
Lead poisoning among children in the United States is almost invariably
caused by repeated ingestion of chips and flakes of lead containing paint and
plaster from the walls, windowsills, and woodwork of pre-World-War-II
houses. It has a high incidence only among children living in city slums,
where accessibility to flaking and peeling lead paint and broken plaster, lack
of knowledge among parents that ingestion of lead paint is dangerous and
even lethal, frequent inadequate parental supervision of young children, and
a high incidence of pica (an appetite for nonfood items such as dirt, paper,
paint, and plaster) all favor lead poisoning.
EXTENT OF PROBLEM
Children under 6 years of age are the main victims and those between 1
and 3 years comprise 85 to 90 percent of the childhood cases.75 Boys and
girls are affected equally. Lead poisoning occurs year round, but lead en-
cephalopathy (brain injury caused by lead), a very serious complication, is
much more frequent during the summer. Some cases have been reported in
winter when leaded battery casings are burned for fuel and the fumes are
inhaled or when there is prolonged contact with the ashes.
Nobody knows exactly how many children in the United States are
exposed to this health hazard, or how many are actually poisoned, for many
cases of childhood lead poisoning go undiagnosed. Since the problem is
closely related to poor housing conditions, an educated guess could be based
on the number of old, deteriorating houses in the United States and the
known rate of lead poisoning among children living in such houses. Ac-
cording to the 1960 Housing Census, 7.5 million of the occupied housing
units in the United States built in or before 1939, when lead paint was
commonly used on interiors, were classified as deteriorating or dilapidated.
Approximately one-eight of the population, or 1.25 million children ages 1
to 3 years old, lives in these houses.75
Although since the 1940's lead pigment has been replaced by titanium
in interior paints, recent surveys in Baltimore, Philadelphia, and Minneapolis
revealed selected slum areas where from 40 to 80 percent of houses still
contained quantities of flaking lead paint. Among children ages 1 to 6 years,
10 to 25 percent living in high-risk areas are found to have higher than
25
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normal blood-lead levels and 2 to 5 percent have clinical symptoms of lead
poisoning. The latter projected to a national level represents roughly 40,000
children, ages 1 to 3 years old.75
Effects of Childhood Poisoning
Until the advent of chelating agents-therapeutic agents that bind the
lead ions and increase their excretion rate—about two-thirds of the children
with lead encephalopathy died. Even with the use of chelating agents, the
fatality rate remained 30 percent for many years. More recently, with the
use of the chelating agents and supportive therapy, the fatality rate has been
reduced to less than 5 percent; but many of the survivors are left severely
handicapped.
In Chicago a follow-up study of 425 children who were treated for lead
poisoning revealed that 165 had some kind of neurological sequela. Among
the 59 children in this group who had symptoms of lead encephalopathy
before treatment, 48 were left with various handicaps: 32 had recurrent
seizures, 22 were mentally retarded, 8 had cerebral palsy, and 4 had optic
atrophy.76
Epidemiological studies in Queensland, Australia, have demonstrated a
high incidence of chronic kidney disease among patients who had lead poi-
soning in childhood 10 to 40 years previously. Half of these patients with
kidney damage also suffered from gouty arthritis, and many had severe high
blood pressure, mental impairment, and psychiatric disorders.77 A similar
study in the United States did not find this high incidence of chronic renal
disease and pointed out that the Queensland cases were not typical of those
seen in the United States.78
Detection Difficulties
Clinical lead poisoning in children is prevalent only among families who
are least able to improve their living conditions and who are not generally
well-informed. The well-informed segments of the population are seldom
affected. Many health agents who work among the poor are not aware that
lead poisoning in children is still a problem. Childhood lead poisoning is a
disease that health workers may not recognize, even though it exists in
epidemic proportions, because it has no distinctive clinical features. Signs
and symptoms of lead poisoning such as anemia, anorexia, abdominal pain,
constipation, increased irritability, and vomiting can all be easily mistaken as
manifestations of other childhood illnesses.
Unless a physician inquires specifically as to whether the child has eaten
chips of paint or plaster and draws a blood specimen for lead determination,
he is likely to miss the diagnosis altogether. He may treat the child for
something else, only to be confronted later with the same patient, who may
then exhibit signs of brain injury which may already be irreversible. The
26 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
-------
probability of this happening is supported by the fact that in some cities
with a high incidence of lead poisoning, certain hospitals serving children
from known "lead belts" report few or no cases of the disease.75
Inadequacy of Housing Codes
Many cities, where lead poisoning is a public health problem, do not
have health or housing codes adequate to protect tenants from exposure to
lead paint. Even in cities with codes specifically prohibiting lead paint in the
interior of dwellings, enforcement of such codes is generally far from satis-
factory. Where city officials are interested in enforcing codes, they fre-
quently do not have enough inspectors and sanitarians to carry out the
necessary procedures for enforcement—inspection of houses, collection of
paint specimens, testing for lead content, and reinspection.75
Another reason housing codes are not an effective solution is that en-
forcement relies primarily on the criminal process, usually in the form of
misdemeanor prosecution in the lower criminal courts where procedural and
conceptual difficulties can delay action indefinitely.
The recurrence rate of lead poisoning is high. Failure to remove lead
paint from a house where a child is known to have developed lead poisoning
usually means that a treated child returns to the same environment to be
exposed again. Among survivors of acute lead encephalopathy who are re-
exposed to an environment that contains lead paint, the incidence of severe
permament brain damage is almost 100 percent.75 Development of inexpen-
sive methods for paint covering and removing is essential.
PROPOSED COMMUNITY CONTROL PROGRAM
The public must be alerted to the dangers of eating paint, the symptoms
of lead poisoning, and the course of action to follow when lead poisoning is
suspected. So that they will always have an index of suspicion, physicians,
nurses, social workers, and all other health workers must also be made aware
of the prevalence of lead poisoning among children. The Surgeon General has
recently stated that lead poisoning should be a reportable disease.
Mass screening programs must be conducted in "lead belts" for all chil-
dren between 1 and 6 years of age. Children found to have elevated body-
lead, levels should be referred to a medical center for further diagnosis and
treatment if necessary. Steps should be taken to prevent their re-exposure to
lead in the home, and all children treated should be re-examined periodically
for possible re-exposure.
Effective health and housing codes concerning lead and lead poisoning
must be established and diligently enforced. Where codes are not enforced,
court action may be necessary.
Lead Poisoning in Children 27
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ECONOMIC CONSIDERATIONS
The estimated cost of treatment and institutionalization to the age of 60
of a person who incurs severe permanent brain damage from lead poisoning
in childhood has been calculated to be around $220,000.79 Complete re-
moval of lead paint from an average rowhouse with 10 windows, two doors,
and baseboard would cost $250 to $300; replacement of window and door
units and baseboards in such a house would cost $600 to $1,200. These
figures show only the difference in dollar costs between preventing lead
poisoning through paint removal and permitting severe brain damage to
occur in children. They do not take into consideration the intangible loss of
useful or potential manpower.
CURRENT STATUS
Many comprehensive health care projects for children sponsored by the
U. S. DHEW Children's Bureau include programs to control lead poisoning.
Pilot projects are currently operating at the Hill Health Center in New
Haven, Connecticut, the Children's Hospital of the District of Columbia; and
several community hospitals in New York City and Chicago. Volunteer
groups are also working in Baltimore, New York, Chicago, New Haven,
Cleveland, and the District of Columbia.74
In 1969, the Lead Industries Association published a booklet entitled
"Facts About Lead and Pediatrics," in which seven steps to the prevention of
lead poisoning were presented. The booklet is distributed to physicians, public
health authorities, social workers, city officials, and others who can help
achieve prevention and control of the disease in children.
The Bureau of Community Environmental Management is preparing
guidelines for local childhood-lead-poisoning control programs based on its
own active collaboration with several communities. These guidelines should
be published in 1971. The Bureau is also supporting studies at the University
of Minnesota on lead metabolism following single doses and at the John
Hopkins University on sequelae of lead encephalopathy and lead poisoning
treatment with chelates.
The Comprehensive Health Care for Children and Youth Program of the
Health Services and Mental Health Administration supports demonstration
community action programs against lead poisoning in Chicago and New York
City. They also support research on the development of improved screening
methods.
The Johns Hopkins University School of Medicine has received a grant
from the U. S. DHEW Children's Bureau to do an urgently needed study of
tests used in screening children for lead poisoning. The goal is to develop a
simple, quick method of determining the amount of lead in human blood for
use in large-scale screening programs. At present, a physician or skilled
28 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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technician must puncture the vein to draw enough blood for blood-lead
determination. The successful testing of more than 120,000 children in
Chicago is evidence that this method of screening for lead poisoning is
feasible on a large scale. Scientists are, however, seeking a quicker, but
equally reliable, method that will require only the small amount of blood
obtained from a finger prick.
Lead Poisoning in Children 29
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34 ENVIRONMENTAL LEAD AND PUBLIC HEALTH
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