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

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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

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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

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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

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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

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    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

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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

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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

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      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

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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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