EPA's POSITION ON THE HEALTH
EFFECTS OF AIRBORNE LEAD
Prepared by
Health Effects Branch
Processes and Effects Division
Office of Research and Monitoring
U. S. Environmental Protection Agency
401 M Street, S.W.
Washington, D. C. 20460
November 29, 1972
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TABLE OF CONTENTS
I. Introduction
II. Clinical Manifestations of Lead Poisoning
III. Low Level Metabolic Effects of Lead
IV. What is a Safe Blood Lead Level?
V. Sources of Lead Exposure Among the General Population
VI. Extent of Abnormal Lead Exposure Among the General Population
VII. Findings and Recommendations
APPENDIX A - Overview of EPA's Conclusions Regarding Responses Received
to Questions which Appeared in the Federal Register
APPENDIX B - A. Survey of Air and Population Lead Levels in Selected
American Communities (Seven City Lead Study)
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I. INTRODUCTION
On February 23, 1972, the Environmental Protection Agency
published fuel additive regulations which would result in the reduction
of lead in gasoline by 60-65% beginning January 1, 1977. The original
health effects papers supporting this decision have been previously
7 "\ 4 R
described/"3'^'0
Following this announcement the Agency solicited public comment on
the proposed regulation. A 90 day comment period was initiated and public
hearings on this question were held in Washington, D.C. (April 11-12, 1972),
Dallas, Texas (April 27-28, 1972), and Los Angeles, California (May 2-4,
1972). Additional comments were solicited in the form of questions which
appeared in the Federal Register.
Many opinions were expressed both by testimony at the hearings and
by written submission immediately following the hearings and during this sub-
sequent extended comment period. All comments received were read and evalu-
ated. The entire hearing record and submitted comments are available for
public inspection at the Environmental Protection Agency in Washington, D.C.
The purpose of this paper is to update the Agency's health position
related to control of lead emissions from motor vehicle exhaust based
upon the most recent information available to EPA, including the Public
Hearing testimony, written comments which were received, and reevalua-
tion of existing data. Since this document focuses primarily upon the
possible direct and/or indirect effects of airborne lead and lead in
gasoline upon man, it is recognized not to represent a balanced
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1-2
comprehensive review of all that is known about the biophysiology of
lead in relation to man. Further, although this paper is meant to be
read primarily by members of the scientific community we have also
endeavored to make it understandable to the lay public. This document
will be considered by EPA in evaluating the health issues that pertain
to its proposed fuel additive regulations.
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1-3
REFERENCES FOR SECTION I -INTRODUCTION
1 Federal Register, Vol. 37, No. 36, pp. 3882-3884, February 23,
1972.
2
"Health Hazards of Lead," EPA, Research Triangle Park, N.C.,
February 23, 1972.
3"Health Hazards of Lead (Revised April 11, 1972)," EPA, Research
Triangle Park, N.C., April 11, 1972.
4
"Atmospheric Lead and Public Health," EPA, Research Triangle Park,
N.C., April 11, 1972.
I
"Corrections and Additions to Health Hazards of Lead (Revised
April 11, 1972)," EPA, Research Triangle Park, N.C., April 27, 1972.
6Federal Register, Vol. 37, No. 115, pp. 11786-11787, June 14, 1972.
7Federal Register, Vol. 37, No. 36, pp. 3882-3884, February 23, 1972.
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II. CLINICAL MANIFESTATIONS OF LEAD POISONING
Lead is a known toxic substance for which no beneficial biological
role'has yet been demonstrated. Effects of severe lead intoxication at
high exposures have been recognized for centuries. These include death
1 p
and irreversible neurological impairment. '
Symptoms of mild lead intoxication include loss of appetite,
irritability, drowsiness, apathy, and abdominal pain. Since these
symptoms are commonly found in many other diseases, the possible role
that lead may have played in their origin is sometimes difficult to
evaluate. These symptoms by themselves cannot be used to imply an
effect caused by lead.
In view of the uncertainty in defining the presence of mild lead
poisoning symptoms, some clinicians and health departments consider
children with abnormally elevated blood leads as "asymptomatic" lead
poisoning cases even if no symptoms or signs of lead intoxication are
evident. Since subtle indications of lead poisoning are difficult to
detect, perceptiveness of both parents and physicians is an important
factor influencing whether symptomatic lead poisoning cases are
identified. Hence, the distinction between excessive lead absorption
and mild lead intoxication is sometimes unclear. For example, children
considered initially to have no symptoms of lead poisoning have been
found, on follow-up medical examinations, to be mentally retarded. In
such instances, however, mental retardation may have been present
before lead poisoning occurred.
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II-2
In one large survey involving 425 children with lead poisoning,
attributed primarily to ingestion of lead based paint, a large percentage
(39%) showed evidence of nervous system damage during follow-up
3
examinations. Mental retardation and recurrent seizures were the
t
most common and persistent findings. In this same study, of 232
children with symptoms of lead poisoning characterized initially by
gastrointestinal complaints, but not by evidence of neurologic damage,
19% were later found to be mentally retarded and 13% to have convulsive
disorders. Whether convulsions were observed only in children with
mental retardation is uncertain from the article. Of 58 children treated
for asymptomatic lead poisoning, five (approximately 10%) were found
during follow-up studies to be mentally retarded. Again, one cannot
rule out the possibility that mental retardation was present before
these children were poisoned by lead.
4
In another study eleven children who had been treated for lead
poisoning attributed primarily to paint were reexamined 5-10 years
later. Mental deterioration was not always obvious and physical and
laboratory tests in general did not reveal abnormalities. However,
specialized tests of visual motor performance indicated subtle brain
damage in the majority of cases.
Several parents of children with blood leads of 50ug/100g and above
have reported improvements in their child's behavior and language ability
following treatment with drugs that removed lead from their bodies, even
though the children had originally been considered asymptomatic cases of
5
excessive lead exposure. Although these were subjective findings which
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II-3
were not compared to those from a matched control group, they do suggest
the possibility that central nervous system damage was present, but
previously undetected in these children.
The possibility that blood lead elevations even at levels generally
not considered excessive (40ug/100g and below) may be associated with
childhood behavioral disturbances such as hyperactivity has recently
been reported. Hyperactive children were observed to have higher
blood lead levels as well as increased post-penicillamine urinary lead
excretion levels compared to a reasonably matched control group. Both
the hyperactive and the control group were similar with respect to age
and sex. However, possible socioeconomic and racial differences
between the groups may have partially confounded these results. Although
blood leads in the hyperactive group were predominantly below 40ug/100g,
urinary lead excretions were abnormally elevated in over 60% of these
children compared to 21% in the control group. Hence, exposure to lead
in quantities presently not considered to be toxic or even excessive may
contribute to minimal brain damage as in the hyperactive syndrome. Since
a history of lead exposure (but apparently not lead poisoning) was more
frequent among the hyperactive children, increased lead exposure early in
childhood may, in certain of these children, have contributed to the
eventual development of hyperactivity problems.
Findings such as these cause speculation, in the opinion of EPA,
that children may be suffering subtle but unrecognized neurological
impairments due to lead.
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II-4
REFERENCES FOR SECTION II - CLINICAL MANIFESTATIONS OF LEAD POISONING
McLaughlin, M. C.: "Lead Poisoning in Children in New York City,
1950-54: An Epidemiologic Study," NY State J Med 56:3711-3714, 1956.
2
Chisolm, J. Julian: "Chronic Lead Intoxication in Children,"
Develop Med Child Neurol 7:529-536, 1965.
3
Perl stein, M. A. and Attala, R.: "Neurologic Sequelae of Plumbism
in Children," Clin Ped 5:292-298, 1966.
n
Thurston, D. L.; Middelkamp, J. N., and Mason, E.: "The Late Effects
of Lead Poisoning," J Ped 47:413-423, 1955.
5
Sachs, H. K.; Blanksma, L. A.; Murray, E. F., and O'Connell, M. J.:
"Ambulatory Treatment of Lead Poisoning: Report of 1,155 Cases," Ped 46:
389-396, 1970.
601iver,D.; Clark,J.; and Voeller, K.; "Lead and Hyperactivity,"
Lancet, pp. 900-903, Oct. 28, 1972.
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HI. LOW LEVEL METABOLIC EFFECTS OF LEAD
Lead is known to interfere with enzyme systems at blood lead
levels lower than those generally associated with clinical symptoms
of lead intoxication. This is especially true for enzymes
containing sulfhydryl groups which are particularly sensitive to
lead.
Delta aminolevulinic acid dehydrase (ALAD), an enzyme involved
in hemoglobin synthesis, is the best documented example of lead
2
enzyme inhibition in man. Measurable increases in urinary ALA resulting
from ALAD inhibition are generally not found until blood lead levels
have reached 40ug/100g. A panel of the National Academy of Sciences
concluded that, at blood lead levels of 40ug/100g and above, inhibition
3
of this enzyme is physiologically significant.
The true significance of ALAD inhibition in man is at present
unclear. Inhibition of ALAD by lead in peripheral blood by itself may
not be clinically important, especially since these reports are based
upon in vitro biochemical determinations which may not accurately reflect
what is happening in man. However, lead induced inhibition of ALAD
required for cytochrome synthesis in other tissues may reflect a
more significant impairment.
For example this inhibition has been demonstrated to occur in
brain, kidney, liver and spleen of suckling rats lead poisoned by
4
maternal milk. ALAD activity in the blood of the suckling rats was
observed to correlate with ALAD activity in the brain. These results
suggest that ALAD inhibition in peripheral blood of children, which occurs
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III-2
at blood lead levels in the 20-40ug/100g range, may be associated with
similar biochemical abnormalities in the brain. Whether this actually
occurs in man, however, is at present unknown.
Inhibtion of enzymes involved in cellular energy production may
partially explain the mechanism by which lead exerts its toxic effects.
The central nervous system is especially sensitive to oxygen deprivation,
and thus could conceivably be extremely sensitive to possible enzyme
inhibition by lead. In this context even slight but sustained eleva-
tions of blood leads may cause subtle, though appreciable, impairment
of central nervous system functions.
Lead has also been recently associated with the possible development
of chromosomal abnormalities in man. Muro and Goyer first reported
5
evidence of experimental chromosomal damage caused by lead in 1969.
In this study chromosomes derived from leukocyte cultures of mice fed
1% lead acetate in their diets demonstrated increased gap-break aberrations.
The authors of the study concluded that similar aberrations in somatic
cells would result in impaired growth. Should these disturbances be
shown to occur in germ cells they would be of potential genetic signi-
ficance. Since this finding, chromosomal abnormalities have been
discovered in the lymphocytes of lead poisoned men and in the lympho-
cytes of workers currently occupationally exposed to lead but not in
former lead workers no longer occupationally exposed. In a community
located near a lead smelter, chromosomal abnormalities were found in
o
13 of 15 randomly selected exposed individuals.
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We do not know whether these effects are associated with low level
chronic lead exposures among the general population. Although these
studies are not by themselves conclusive, they indicate that we
should be concerned about possible genetic implications resulting from
general population exposures to lead.
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III-4
REFERENCES TO SECTION III - LOW LEVEL METABOLIC EFFECTS OF LEAD
T
Hernberg, S.; Nikkanen, J.; Mellin, G.; and Lilius, H.:
"Delta Aminolevulinic Acid Dehydrase As a Measure of Lead Exposure,"
Arch Environ Health 21:140-145, 1970.
2
Ibid.
3
"Airborne Lead in Perspective", A report prepared by the Committee
on Biological Effects of Atmospheric Pollutants of the Division of Medical
Sciences, National Research Council, National Academy of Sciences,
Washington, D. C., 1972, p.110.
4
Millar, J. A.: Battistini, V.; Cumming, R. L., et al: "Lead
and Delta Aminolevulinic Acid Dehydratase Levels in Mentally Retarded
Children and In Lead-Poisoned Suckling Rats," Lancet 2:695-698, 1970.
5
Muro, L. A. and Goyer, R. A.: "Chromosome Damage in Experimental
Lead Poisoning," Arch of Pathology 87:660-663, 1969.
6
"Airborne Lead in Perspective", op.cit., p.166.
7
Form', A. and Secchi, G.: "Chromosomal Changes in Preclinical and
Clinical Lead Poisoning and Correlation with Biochemical Findings," (preprint)
presented at the International Symposium on Environmental Health Aspects
of Lead, Amsterdam, October 2-6, 1972.
8
Graovac-Leposavic, L.: Djuric, D.; Valjarevic, V.; Senicar, H.;
Senicar, L.; Milic, S.; and Delic, V.: "Environmental Lead Contamination
of Meza Valley - Study on Lead Exposure of Population," (preprint) presented
at the International Symposium on Environmental Health Aspects of Lead,
Amsterdam, October 2-6, 1972.
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IV. WHAT IS A SAFE BLOOD LEAD LEVEL?
Blood lead levels are frequently used and generally accepted as
indices of lead exposure both in the general population and in occupa-
tional health situations. Much uncertainty still exists as to the
precise relationship between any given blood lead level and the total
amount of lead stored in the body. Blood lead levels are probably a
function not only of the total body lead stores, but also of the degree
of recent lead exposure from all sources including food, water and air.
Although much emphasis in this paper is placed upon blood lead as an
indicator of exposure, as well as associated risk due to lead, one must
recognize that blood lead may not always be an accurate reflection of
either situation. Our reason for employing blood lead as the primary
exposure index in this document is that, in our opinion, it is presently
the best available index that can be related to the possible
development of clinical effects due to lead.
Establishment of a single safe blood lead level protective of all
high risk groups in the general population is not possible with presently
available data. A range of individual responsiveness to lead probably
occurs in both children and adults. Healthy adults usually do not
demonstrate symptoms of lead intoxication until blood leads have reached
80ug/100g, although symptoms have been reported at blood lead levels in
2
the 50-80ug/100g range. Blood lead levels considered safe for adults
may not always be safe for children. For example, clinical symptoms of
lead intoxication often occur at lower blood lead levels in children
than in adults.
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IV-2
Lead poisoning cases among children are most common in the 1-3
year old age category. This may reflect increased lead exposure among
this group due to ingestion of non-food objects containing lead. This
ingestion might occur during the normal developmental stage of oral
exploration or as a result of an increased incidence of pica at this age.
The borderline between abnormal non-food ingestion (pica) and routine
oral exploration in children is difficult to define. The possibility
that young children may absorb more lead from the oral route than older
children and adults is an alternative explanation for the observation
that more lead poisoning occurs in 1-3 year olds. Recent data suggest
that healthy children may absorb as much as 50% of their oral lead
intake compared to the commonly accepted figure of approximately 10%
in adults. The possibility that there may actually be an increased
biological response to a given internal level of lead in young children
must also be considered an alternative and/or contributing factor
explaining why lead poisoning is more common in young children. The
point of view that children and the young of any species may be more
susceptible to lead has been supported by a number of workers in the
field.4'5
In recognition of the possibility that young children may be
more susceptible to lead than older children and adults, the newborn and
the fetus would be expected to be especially vulnerable to lead.
Exposure of the developing central nervous system in utero to lead, an
established neurotoxic agent, should thus be kept at a minimum. The
conservative point of view favors a reasonable safety factor between
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IV-3
what is considered an acceptable lead exposure among the fetus and
newborn compared to older children and adults.
-Most scientists in the field of lead including those from two
leading manufacturers of lead additives, the Ethyl Corporation and
DuPont, are in agreement with acceptance of 40ug/100g as the upper accept-
able blood lead level for adults in the general population. ' Blood
lead levels above 40ug/100g in adults are thus usually considered evidence
that excessive exposure to lead has occurred. In children, the blood
lead level generally considered to be evidence of excessive lead exposure
8910
has also been established at 40ug/100g. ' ' Since children are
probably more susceptible to lead than adults, one must consider the
desirability of revising this figure downward to some level below 40ug/100g.
An upper acceptable individual blood lead level in children of 35ug/100g
has in fact recently been proposed.
Cases of lead poisoning have been reported among children with blood
lead levels in the 40-50ug/100g range.12'13'14'15 Relating the onset
of clinical symptoms of lead poisoning to any specific blood lead level
is, of course, recognized to be difficult. The possibility that blood
lead is being measured at a point in time when the child is actually
asymptomatic must be considered. Such a situation would result in
attributing symptoms of lead poisoning to a blood lead level lower than
had actually existed when symptoms had initially occurred. As a result,
many workers in the field are reluctant to routinely attribute possible
symptoms of lead poisoning in children to blood leads in the 40-50ug/TOOg
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IV-4
range. However, one should also recognize that since symptoms of mild
lead poisoning in children are so difficult to identify, the possibility
that clinical disease and/or borderline functional impairments may
occur at blood lead levels in the 40-50ug/100g range and below has not
yet been adequately ruled out. Should many children be shown to have
blood lead levels in the 40-50ug/100g range, the need to reduce lead
exposures wherever and whenever possible due to the large number of
children conceivably affected may greatly outweigh any uncertainty in the
observation itself.
As stated above the prudent position is to recommend establishment
of a reasonable safety factor between what is considered an acceptable
blood lead level in the fetus and newborn in comparison to older children
and adults. On this basis, we suggest that umbilical cord blood lead
levels of 30ug/100g and above for the newborn and the fetus be considered
abnormally elevated. This reflects probable vulnerability, of the
developing central nervous system to lead, an established neurotoxic
agent. This recommendation must, of course, be viewed as a judgement
which has not yet been adequately validated by scientific studies.
Compared to adults, newborn babies generally have elevated
hematocrits. Since approximately 90% of blood lead is believed bound
to the red blood cell, in theory a blood lead level of 30ug/100g in a
newborn is really equivalent to a lower blood lead in adults based upon
this hematocrit correction. However, the fact that the newborn has a
higher proportion of circulating blood volume in comparison to body mass
than adults could compensate to some extent for this hematocrit difference.
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IV-5
In addition, the larger mass of central nervous system tissue and the
smaller mass of skeletal tissue in the newborn per unit of body weight
compared to adults, as well as the relative immaturity of the blood
brain barrier at birth are additional factors favoring a margin of safety
between what is considered an upper acceptable blood lead in the
newborn as compared to older children and adults.
In the opinion of EPA, the available information supports the
position that to provide adequate assurances of safety, upper acceptable
blood lead guidelines for the general population should be defined
as shown in Table IV-1. Blood lead levels above these guidelines in
individuals do not necessarily indicate that clinical disease is actually
present. These guidelines reflect a judgmental decision with regard to
which levels of lead exposure may be associated with a greater possible
occurrence of adverse clinical and/or subclinical effects.
For the fetus and the newborn the upper acceptable blood lead
limit should be 30ug/100g; for children it should be no more than
40ug/100g (possibly 35ug/100g). In adults a blood lead level of 40ug/100g
or above should be considered abnormal and evidence of excessive lead
exposure. For expectant mothers a blood lead level of 30ug/100g or
above may be a potential hazard to her newborn infant since blood lead
levels in newborns are dependent upon and correlate well with maternal
16
blood lead levels.
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IV-6
TABLE IV-1
Blood Lead Guidelines in the General Population
Upper Acceptable Blood Lead Level
Group (ug/lOOg)
Fetus and Newborn 30
Children No more than 40
Adults 40
Expectant Mothers 30
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IV-7
REFERENCES FOR SECTION IV - WHAT IS A SAFE BLOOD LEAD LEVEL?
Lin-Fu, Jane S.: "Medical Progress - Undue Absorption of Lead
Among Children - A New Look at an Old Problem," New Eng J Med, 286:
702-710, March, 1972.
p
Airborne Lead in Perspective," National Academy of Science,
Washington, D. C., 1972, p.94.
Alexander, F. W.; Delves, H. T.: and Clayton, B. E: "The Uptake
and Excretion by Children of Lead and Other Contaminants," (preprint),
paper presented at International Symposium on Environmental Health
Aspects of Lead, Amsterdam, October 2-6, 1972.
4Ibid.
5Lin-Fu, op.cit.
Supplement, comment of Ethyl Corporation on EPA's Proposed Lead
Regulation, Ethyl Corporation, July 13, 1972, p.12.
Diggs, D.E: letter to the Deputy Assistant Administrator for
Air Programs, EPA, in "Supplemental Statement by E.I. DuPont De Nemours
and Company, Inc., Relative to EPA Request for Additional Information on
the Health Effects of Airborne Lead," July 12, 1972.
8"Medical Aspects of Childhood Lead Poisoning," HSMHA Health Reports,
86:140-143,1971.
q
Lin-Fu, op.cit..
10Chisolm, J. J: Testimony submitted to EPA, July 26, 1972.
Zielhuis, R: "Lead Absorption and Public Health: An Appraisal of
Hazards,: (preprint), paper presented at International Symposium on
Environmental Health Aspects of Lead, Amsterdam, October 2-6, 1972.
12
Jacobziner.H: "Lead Poisoning in Childhood: Epidemiology,
Manifestations and Prevention," Clin Ped 5:277-286, 1966.
13
Moncrieff, A; Koumides, 0; Clayton, B; et al: "Lead Poisoning
in Children," Arch Dis Child, 39:1-13, 1964.
14
Freeman, R: "Chronic Lead Poisoning in Children: A Review of
90 Children Diagnosed in Sydney, 1948-1967, Australian Ped J, 5:27-35,
1969.
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IV-8
15
Berman, E: "The Biochemistry of Lead: Review of the Body
Distribution and Methods of Lead Determination," Clin Red, 5:287-291,
1966..
16
Haas, T, et al: "Research on the Ecological Lead Burden During
Childhood," (preprint), Paper presented at International Symposium on
Environmental Health Aspects of Lead, Amsterdam, October 2-6, 1972.
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V. SOURCES OF LEAD EXPOSURE AMONG THE GENERAL POPULATION
Man is exposed to lead primarily through the food he eats, the
water he drinks and the air he breathes. Children, especially those
with pica, (habitual ingestion of non-food objects) are exposed to lead
not only via air, food, and water, but may also be exposed through
ingestion of lead contaminated paint, dirt, and dust. Lead contaminated
dirt and dust are readily available for children to ingest. Possible
exposure of children to lead contaminated paint, dirt and dust is
particularly significant for all children, even those without pica, who
may ingest these substances during the normal developmental phase of
oral exploration.
Fallout of lead from the air is a significant contributor to the
lead present in dirt and dust found in urban streets, parks, and homes.
Airborne lead is in turn directly related to the use of lead as a gasoline
additive. Over 90% of airborne lead emissions in the United States are a
result of leaded gasoline combustion. Hence, levels of lead in dust
and dirt, especially in urban areas are a function of the use of lead
additives. This position is supported by the observation that average
soil lead levels collected in front yards of homes in urban areas are
two to three times greater than soil lead concentrations in back yards
2
which are located further away from roadways. Preliminary data also
indicate that levels of lead in housedust from middle class homes in
urban areas are roughly double those found in housedust from middle
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V-2
class homes in suburban areas. Levels of lead in housedust exceeding
0.06% were reported in these urban homes. Use of lead as a gasoline
additive is believed to be a significant factor contributing to this
difference and is consistent with the established decrease of lead
4
fallout from the air with increased distances from roadways as well as
the higher levels of lead fallout observed in commercial areas compared
5
to residential areas.
The potential contribution of air lead exposures to blood lead in
the general population remains a significant issue of debate within the
scientific community. While many investigators continue not to support
the position that community air lead exposures especially at or below
3
2ug/m are capable of affecting blood lead levels in adults residing in
the general population, EPA believes that recently completed studies
indicate that blood leads are affected. The frequently discussed "Seven
City Lead Study" has often been cited as evidence in support of the
q
view that low air lead levels (around 2ug/m ). do not have an effect upon
blood lead. EPA is not in agreement with this interpretation since
depending upon the method of data analysis, effects of air lead at these
exposures on blood lead levels can be demonstrated. For example, although
a good correlation between air lead and blood lead was not obtained when
all geographic areas were considered together, females residing in urban
areas and exposed to higher air lead levels were consistently found to
have higher blood lead levels than females residing in suburban areas.
These issues are discussed more fully in Appendix B. This finding may
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V-3
be most significant in terms of the potential impact that higher
blood lead levels in mothers may have upon blood lead levels among
their newborn babies.
One can never be completely certain that increased blood lead
levels in female urban residents are entirely due to increased air lead
exposures. Other factors such as dietary lead differences as well as
the possibility that lead content of water is higher in urban areas
may also be contributing. Nevertheless, the consistent blood lead
increments found in areas of greater air lead exposure suggests that
air lead may be a factor and a factor which may be easily controlled.
Recent reports of significantly increased blood lead levels among
women residing in homes in close proximity to a well traveled roadway
compared to those living greater distances from that roadway add support
to the possibility that air lead resulting from combustion of gasoline
containing lead additives is a factor capable of increasing blood lead
levels in urban communities. Blood lead level differences among groups
reported in this study were probably not significantly affected by
either dietary or water lead differences since all women studied
presumably had reasonably common sources for both diet and water.
Further, the air lead exposures in this investigation were measured
inside the homes and on the front porches of the homes of the women
studied. This represents a much more accurate determination of true
air lead exposure than those from the "Seven City Study" where measure-
ments were made at air sampling stations much further distances away
(as great as one mile) and sometimes at heights far above ground level.
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V-4
Of particular note is the fact that, in the study near the well
traveled road, higher blood lead levels were found in the high exposure
group despite air lead measurements in the homes and in the vicinity of
3
the homes of this group which were only l-2ug/m greater than those from
the low exposure groups. Further, the high exposure group was characterized
not only by statistically significant increases in average blood lead
levels, but also by more women with blood lead levels at or above 30ug/100g
compared to those in the low exposure categories. Although more women
residing in homes 400 feet from the roadway had blood leads above 29ug/100g
than women residing in homes 125 feet from this road, this difference was
not statistically significant based upon a Chi square analysis (0.10< p< 0.20).
However, the increase in number of women with blood leads greater than
29ug/100g in the group living closest to the roadway compared to the groups
living 125 and 400 feet away was statistically significant in each
instance (p<0.01). These results, considered by EPA to be even more reli-
\
able than those from the "Seven City Study" generally confirm similar
observations derived from the "Seven City Study." The following table
summarizes these results.
Comparisons between values obtained from the Seven City Study with
those from the Roadway Study must be made with caution since the groups
may not be matched closely enough with regard to all variables generally
recognized to influence blood lead levels (such as diet, age, race, hema-
tocrit and smoking). However, the comparisons within the Roadway Study
and those within specific urban-suburban areas from the "Seven City Study"
are more valid so that causal inferences appear reasonably justified
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V-5
TABLE V-l
Summary of Data Relating
Place of
Number
Population Studied
From Roadway Study
Living Near Roadway
( 12 feet away)
Living Away From Roadway
(a) 125 feet away
(b) 400 feet away
From Seven City Study
New York Urban
New York Suburban
Chicago Urban
Chicago Suburban
Philadelphia Urban
Philadelphia Suburban
55
34
61
Number
Studied
140
198
147
208
136
150
Average Air
Lead Exposure
(ug/m3)
Front Porch In Home
4.60 2.30
2.41 1.50
2.24 1.57
Average Air Lead
Exposure ug/m3
(geometric mean)
2.08
1.13
1.76
1.18
1.67
1.15
Blood Lead Levels in W
Residence
Average Blood
Lead
ug/lOOg
23.1
17.4
17.6
Average Blood
Lead ug/lOOg
(geometric mean)
16.6
15.3
17.6
13.9
20.5
18.0
%Blood Leads
Above
29ug/100g
25.4
0
6.6
%Blood Leads
Above
29ug/100g
1.
0,
3.4
0.5
11.0
4.7
%Blood
Leads 40
& Above
1.8
0
1.6
%Blood
Leads 40
and Above
0
0
0.7
0
1.5
0
%Blood
Leads
Above 50
1.8
0
0
%Blood
Leads
Above 50
0
0
0
0
0
0
-------
V-6
with respect to the possible impact of air lead upon blood lead.
Although recent theoretical predictions derived from microscopic anal-
yses of lead particulate matter suggest that airborne lead in the general
urban environment might not be appreciably absorbed,via the respiratory
o
route these above data would seem to contradict this position. These data
suggest that even small increments in community air lead exposures have a
definite effect upon blood lead levels among women residing in urban areas.
Further, these results cast doubt on the adequacy of the previous
position taken by EPA that achievement of a.2ug/m air lead goal would
assure a reasonably complete degree of public health protection. This is
especially true in view of the possibility that blood lead levels at or
above 30ug/100g in mothers might cause similar blood lead elevations among
their newborn babies. A statistically significant correlation has been
reported between blood lead levels in mothers and those in their newborn
infants indicating that the concentration of lead in newborns is dependent
Q
upon levels of blood lead in the mother. These observations are supported
by additional studies showing that residence in urban environments is
.associated with elevated blood lead levels ' and that persons living
near highways generally tend to have higher blood lead levels than those
12
living away from highways. This latter study again implicates lead in
gasoline as a factor contributing to these blood lead elevations.
An investigation of blood lead levels in taxi drivers and other
occupational groups, not all occupationally exposed to automobile exhausts,
using personal monitors to measure air lead exposure, is also reasonably
13
consistent with these above observations. Statistically significant
-------
V-7
correlations between air lead and blood lead were not obtained within each
group studied (30 subjects per group). However, when all groups were
combined and adjusted statistically to account for dietary lead differences
among groups, a significant correlation between air lead and blood lead
was obtained. In this latter analysis, variation in air lead exposure
accounted for 44% of the variation in blood lead levels which is reasonable
considering the variation due to dietary lead sources that still existed
within groups. Blood lead levels of 40ug/100g were generally not observed
even in the high exposure group in which air lead measurements reached
3
9ug/m . This may seem to be somewhat contradictory at first. However,
when one considers the small number of individuals studied within each
group (30) the failure to detect blood lead levels of 40ug/100g and above
only rules out the possible occurrence of these high blood lead levels
at a rate of approximately 10% within each group.* Among general urban
*What sample size N is needed to find at least one case
where the prevalence rate is P, with probability 1 - a?
The probability of at least one case is one minus the
probability of no cases:
1 - (1 - P)N
Setting this equal to 1 - a gives
1 _ (i _ p)N = i _ a
N = (log a)/log (1 - P)
for a = 0.05 we have: p
P
P
P
P
= 0.01
= 0.03
= 0.05
= 0.095
= 0.10
N =
N =
N =
N =
N =
299
99
59
30
28.4
-------
V-8
adult populations, blood lead levels of 40ug/100g do not usually occur
more frequently than 5%. These points are discussed in greater detail in
the following section.
Carefully controlled chamber exposures to airborne lead at approxi-
o
mately 3ug/m • in human volunteers also demonstrate that blood lead
14
increments can be expected at these air lead levels. For example, after
3
12 weeks of nearly continuous exposure to air lead at 3.2ug/m, average
blood leads rose more than 30% (from 18.0 to 24.1 ug/lOOg) among a group
of 6 prisoner volunteers who had not been appreciably exposed to airborne
lead since arriving at the prison which was located in a rural environment.
During this study all men had common sources of dietary lead intake.
Although smoking habits may have differed among the men, each man was his
own control and presumably continued to smoke at the same rate during
this study as before. Blood leads returned to pre-exposure levels following
cessation of the experiment. Hence, air lead exposures at approximately
3ug/m appeared responsible for the observed blood lead elevations. These
blood lead increases were comparable to those found among the women re-
siding near a well traveled road. (See Table V-l).
With respect to children, the possible effect of direct air lead
exposures conceivably is of secondary importance when compared to the
role air lead may play in contaminating dirt and dust which could then be
ingested by young children. Elevated blood lead levels have been found
among children attending school in higher air lead areas compared to those
15
in lower air lead areas. The difference in air lead exposure between
3 3
areas (1.69ug/m vs 1.48ug/m ) may have been too small to singly account
-------
V-9
for the entire difference in average blood lead levels which was observed,
(34.1 +9.7ug/100g, mean ^standard deviation, in high air lead area
compared to 26.3 j7.1ug/100g in low air lead area). In this case air
3
lead levels below 2.0ug/m were associated with blood lead levels of
40ug/100g and above in approximately 20% of tested children in the high
exposure area. Since peeling lead paint was not believed to be a signi-
ficant problem in this community, these findings suggest the possible role
that the dustfall lead exposure mechanism may have played in contributing
to these blood lead elevations. Several industrial sources of lead
emissions were present in the vicinity of the homes where these children
lived and could well have contributed to significant fallout of lead from
the air to contaminate dirt and dust.
Previous epidemiologic studies of the lead poisoning problem
among children have consistently associated lead poisoning and excessive
lead exposure with residence in homes containing lead based peeling paint.
Lead based peeling paint is a problem that must be vigorously attacked.
However, associating residence in deteriorating housing containing
peeling lead based paint with lead poisoning does not mean that other
environmental lead sources, such as lead contaminated dirt and dust
are not also contributing to excessive lead exposure among the children
residing in these homes.
Analysis of exising data indicates that environmental exposures
to lead contaminated dirt and dust can contribute significantly to
excessive lead exposure in children. Samples of dirt and dust collected
from the streets of urban areas reveal concentrations of lead far greater
-------
V-10
than those considered safe in paint by the Food and Drug Administration
17 18 19
(0.06%). ' ' These surveys of urban environments in Boston and
Washington demonstrate elevated concentrations of lead in street dirt
at times exceeding 0.5%. Levels of lead in dust were also found inside
20
homes in the Boston area predominantly in the range between 0.1-0.2%.
Although lead from peeling paint may have partially accounted for this
observation in older homes, this factor was not a reasonable explanation
for the elevated housedust lead concentrations often found in homes
built after 1950. Concentrations of lead in street dust of 0.2% and
lead in dust on window frames near busy roadways of 0.175% have also
21
been observed in European cities. Based upon this study, lead
concentrations up to 0.5% are believed common in fine fractions of
street dust collected from busy roadways.
As indicated above, lead contaminated dirt and dust may be
ingested by children. The prevalence of pica (habitual ingestion of
22
non-food items) among children, is high, perhaps exceeding 50%.
While high concentrations of lead in individual paint chips are con-
sidered especially hazardous, cases of lead poisoning in children have
23 24
been associated with paint surfaces containing less than 1% lead.
Data from the City of New York Lead Poisoning Control Bureau indicate
that among children with blood leads betwen 35 and 44ug/100g, only half
25
can be associated with peeling paint containing 1% lead or greater.
Further, nearly 20% of cases in this blood lead category lived in homes
in which peeling paint was not identified.
-------
V-ll
It is well recognized that children may contact peeling lead
oased paint in homes other than their own and that peeling paint
containing 1% or more lead may often be found upon re-inspection of
homes initially not considered to contain this hazard. However, the
presence of lead contaminated dirt and dust (even well below 1% lead)
is also believed to be potentially harmful to children. Continued
ingestion of only fractions of a teaspoon per day of the lead contaminated
dirt and dust presently routinely found in urban areas by children would
easily exceed the well recognized daily permissible intake of lead for
26
children (DPI) established at SOOug lead per day.
For example, lead emitted from automobiles is known to be absorbed
from the gastrointestinal tract under experimental conditions. Rats
fed samples of lead contaminated dirt collected from the Queens Midtown
Tunnel in New York (at 5mg lead per day in their diet), demonstrate
3-4 fold increases in blood lead levels compared to controls not fed
27
this material. Combined ingestion of lead based paint and lead in
dirt and dust thus could be responsible for the large number of urban
children found to have abnormally elevated blood leads.
A report by the National Academy of Sciences is in agreement with
this conclusion and states that, "the swallowing of lead contaminated
dusts may well account in large part for the higher mean blood lead
content in urban children and the rather large fraction whose blood lead
28
content falls in the range of 40-60ug/100g."
-------
V-12
The possible role that calcium deficient diets may play in enhancing
gastrointestinal lead absorption is another potentially important factor
that must be considered. Low calcium diets greatly increased lead
absorption and lead body burdens as well as associated lead pathologic
changes in rats fed 200ppm lead in their drinking water compared to
29
controls on normal calcium diets. Calcium deficient, diets also appeared
to alter the partitioning of lead between fixed bone and the more readily
diffusable lead found in soft tissues. These results suggest that
at least under certain metabolic conditions (such as low calcium diets),
lead stored in bone is more readily available for movement to other
tissues. Conditions such as pregnancy, where there is a requirement
for more calcium than usual, might also be associated with a similar
movement of lead from bone unless adequate calcium is supplied. Such
a situation, if it were shown to occur, should be considered potentially
harmful to the fetus.
Since children living in high risk urban areas are often members
of low socioeconomic groups, they might be at risk not only from exposure
to lead based paint and lead contaminated dirt and dust but also by
the possible coexistence of dietary calcium and/or iron deficiencies.
In this context, experimental iron deficiency has also been shown to
produce greater concentrations of lead in tissues of rats given subtoxic
30
levels of lead compared to a similar group of rats without iron deficiency.
Additional studies further support the possibility that the dust-
fall lead exposure mechanism may represent a potential hazard to children.
-------
V-13
In one investigation, 230 rural children and 272 children from an urban
poverty area were tested for excessive lead exposure in the summer of 1971.
Nearly all of the rural children (18 out of 19) with excessive lead body
burdens lived in homes containing at least one accessible surface with
1% lead paint or greater. However, this paint hazard could be found on
accessible indoor and exterior surfaces in homes of only 60% of urban
children found to have excessive lead exposure. Further, approximately
one quarter of the urban children tested had abnormally elevated blood
leads (40ug/100g and above) compared to less than 10% of the suburban
children. Hence, young children living in urban areas appear to be more
excessively exposed to lead than those residing in rural areas. These
findings are consistent with the possibility that excessive lead expo-
sures are caused not only by lead in paint, but also by lead in other
urban environmental sources including lead in the air, and in the dust
and dirt which settles out from the air. The Department of Health,
Education and Welfare, in commenting upon EPA's position regarding removal
of lead from gasoline notes: "For those children with pica who eat dirt,
32
the danger from exposure to lead containing dust and dirt is great."
Demonstration of excessive lead exposures among children residing
near a smelter in El Paso, Texas, further emphasizes the potential
33
importance of the dustfall lead exposure mechanism. Approximately
90% of the 1-5 year old children sampled who were living near the
smelter had blood leads of 40ug/100g or above. Information available to
EPA indicates that lead paint was not a significant factor in the
etiology of abnormally elevated blood lead levels found among children
34
residing near the smelter. Soil lead levels in the vicinity of the
-------
V-14
smelter averaged 0.4%-0.5% lead with a range of 0.15% to just over 1%.
These are not significantly different from levels of lead in dirt and
soils found in many urban streets and parks.
Though air lead levels were also significantly elevated near
o
the smelter (100-300ug/m ), most of the airborne lead (approximately
75%) was judged to be in the nonrespirable range. A larger percentage
(89.2%) of the 1-5 year old children living in the vicinity of the
smelter had abnormally elevated blood leads compared to a 6-17 year old
group residing in the same area (64.7%). This suggests that exposure
to airborne lead as well as ingestion of lead contaminated dusts was
contributing to excessive exposures in the group more likely to ingest
non-food items, the 1-5 year olds. Hence, levels of lead in street dirt
of this magnitude (averaging 0.4-0.5%) found near the smelter
represent a potential hazard for children with pica. A more in depth
study supervised by HEW, with EPA participation, is currently planned
to further clarify the etiology and extent of this problem.
One recent revaluation of lead sources in the environment,
including factors to account for lead concentration as well as
availability of the source considers lead in dirt (but not airborne
lead directly) to represent a potential source of lead approximately
35
one half the magnitude of that from lead in paint.
In summary, blood lead should be considered a function of all
exposure routes. Available evidence indicates that living in urban
environments where lead exposures are generally elevated, is associated
-------
V-15
with higher blood lead levels in adults. Even air lead levels around
3
2ug/m appear to contribute to blood lead levels among adults and may
possibly contribute to elevated blood lead levels among babies born to
mothers living in urban environments. Especially for children who are
known to ingest non-food items, lead falling out from the air and in turn
contaminating dirt and dust should be considered a potential hazard.
Over 90% of airborne lead emissions are a result of leaded gasoline
combustion. Consequently, lead in the air as well as in street dirt
and household dust are preventable exposures which can be readily
decreased by regulating the use of lead as a gasoline additive.
-------
V-16
REFERENCES FOR SECTION V
SOURCES OF LEAD EXPOSURE AMONG THE GENERAL-POPULATION
Office of Air Programs Data File of Nationwide Emissions, 1970,
Environmental Protection Agency, Research Triangle Park, North
Carolina, July, 1972, Table 6-2.
2
Pinkerton, C., Hammer, D. I., Hinners, T. A., Kent, J. L.,
Hasselblad, V., Lagerwerff, J. V., and Ferrand, E. F., "Trace Metals in
Urban Soils and Housedust," paper presented to Environmental Section,
APHA Centennial Convention, Atlantic City, New Jersey, Nov. 16, 1972.
3Ibid.
Creason, J. P., McNulty, 0., Heiderscheit, L.T., Swanson, D. H., and
Buechley, R. W., "Roadside Gradients in Atmospheric Concentrations of
Cadmium, Lead and Zinc," Presented at the Fifth Annual Conference on
Trace Substances in Environmental Health, Columbia, Missouri, July, 1971.
5
Hunt, H. R., Pinkerton, C., McNulty, 0., and Creason, J., "A Study in
Trace Element Pollution of Air in 77 Midwest Cities," Presented at the
4th Annual Conference on Trace Substances in Environmental Health,
Columbia, Missouri, June, 1970.
Tepper, Lloyd, and Levin, Linda, "A Survey of Air and Population Lead
Levels in Selected American Communities," Report submitted to EPA,
June, 1972.
Daines, R. H., Smith, D. H., Feliciano, A. F., and Trout, J. R.,
"Air Levels of Lead Inside and Outside Homes," Ind Med Journal,
41:26-28, October 1972..
Lawther, P., "More Observations on Airborne Lead," (preprint) Paper
Presented at International Symposium on Environmental Health Aspects of
Lead, Amsterdam, October 2-6, 1972.
g
Haas, T., et al, "Research on the Biological Lead Burden During
Childhood," (preprint and abstract), Paper presented at International
Symposium on Environmental Health Aspects of Lead, Amsterdam, October
2-6, 1972.
"Survey of Lead in the Atmosphere of Three Urban Communities,"
Public Health Service Publication, No. 999-AP-12.
-------
V-17
^Hofreuter, D. H., et al. "The Public Health Significance of
Atmospheric Lead," Arch Environmental Health, Vol. 3, November 1961,
pp. 82-88.
12
Thomas, H. V., et al. "Blood Lead of Persons Living Near Freeways."
Arch Environmental Health, Vol. 15 (1967), pp. 695-702.
Azar, A., Habibi, K., and Snee, R., "Relationship of Community
Levels of Air Lead and Indices of Lead Absorption," (preprint) Paper
Presented at International Symposium on Environmental Health Aspects
of Lead, Amsterdam, October 2-6, 1972.
14Knelson, John H.; Coulston, Fredrick; Goldberg, Leon; Griffin, Travis;
and Johnson, Richard, J.: "Kinetics of Respiratory Lead Uptake in
Humans," Paper presented at the International Symposium on Environmental
Health Aspects of Lead, Amsterdam, Netherlands, October 2-6, 1972. (preprint)
Mclntire, M. and Angle, Carol R., "Air Lead: Relation to Lead in
Blood of Black School Children Deficient in Glucose 6--Phosphate
Dehydrogenase," Science, Vol. 177, August 1972, pp. 520-522.
16Shy, C., Hammer, D., Goldberg, H., Newill, V. and Nelson, W.,
"Health Hazards of Environmental Lead," DHER In-House Technical Report,
EPA, Research Triangle Park, N. C., March 1971.
17Krueger, H., Boston, Mass. Testimony submitted to EPA July 10, 1972.
^Fritsch, Albert and Prival, Michael, Center for Science in the
Public Interest. Testimony submitted to EPA, 1972.
19Duval, Merlin, Asst. Sec. Health and Scientific Affairs, DHEW.
Testimony before the Senate Subcommittee on Health, March 10, 1972.
on
Krueger, H., Boston, Mass. Testimony submitted to EPA July 10, 1972.
PI
Rameau, J., "Lead as an Environmental Pollutant," (preprint) Paper
presented at International Symposium on Environmental Health Aspects of
Lead, Amsterdam, October 2-6, 1972.
22Lin-Fu, Jane. "Lead Poisoning in Children," Children's Bureau
Publication No. 452-1967, DHEW (1967).
23Guinee, Vincent. "Lead Poisoning," American Journal of Medicine,
Vol. 52 (1972), pp. 283-288.
4Guinee, Vincent. Testimony before Subcommittee on Health of the
Committee on Labor and Public Welfare, United States Senate, March 9,
1972. (Position of New York City on the Control of Childhood Lead Paint
Poisoning.)
-------
V-18
25
NYC Bureau of Lead Poisoning Control*data submitted to EPA,
August 31, 1972 and September 12, 1972.
26
King, Barry G., "Maximum Daily Intake of Lead Without Excessive
Body Lead Burden in Children," Amer. Journal Dis. Child., 122:pp.337-340.
October, 1971.
07
Stara, J. F., Moore, W. and Bridbord, K., "Blood and Tissue Levels
in Rats Fed Dust Containing Environmentally Bound Lead," Report of
preliminary data from Environmental Toxicology Division, EPA,
Cincinnati, Ohio.
28
"Airborne Lead in Perspective," National Academy of Sciences,
Washington, D. C., 1972, p. 139.
29
Six, Kathryn, and Goyer, Robert, "Experimental Enhancement of Lead
Toxicity by Low Dietary Calcium," J. Lab. and Clin. Med., 76:933-942, 1970.
Six and Goyer, "The Influence of Iron Deficiency on Tissue
Content and Toxicity of Lead in the Rat," J. Lab. and Clin. Med. 79:
pp. 128-136, 1972.
Lepow, Martha. Testimony before Senate Committee on Commerce,
Subcommittee on the Environment, Washington, D. C., May 8, 1972.
32Richardson, Elliot, Secretary, DHEW. Letter to EPA Administrator
William D. Ruckelshaus, August 11, 1972.
33
Chisolm, J. Julian. Letter to James M. Simpson, June 29, 1972,
and information submitted to EPA July 17, and 26, 1972.
34Ibid.
35
Barltrop, D., "Sources and Significance of Environmental Lead for
Children," (Preprint) Paper presented at International Symposium on
Environmental Health Aspects of Lead, Amsterdam, October 2-6, 1972.
-------
VI. EXTENT OF ABNORMAL LEAD EXPOSURE AMONG THE 'GENERAL POPULATION
Individuals within groups may often be excessively exposed to lead
even though average lead exposures for the group are well within normal
limits. Thus, although average blood lead levels among urban populations
are well within normal limits, considerable numbers of individual urban
residents have blood lead levels exceeding 40ug/100g.
Abnormal blood level elevations have been documented among adults.
They are usually associated with residence in urban areas where air lead
levels tend to be greatest. At present, it is unclear whether increased
air lead exposures in urban areas are solely responsible for these blood
lead elevations. Other sources, such as increased dietary lead and water
lead, might be alternative explanations. Ingestion of water containing
lead immediately above the PHS standard of 50ug/l would not generally
increase ingested lead intake much above that expected as a result of normal
dietary variability (100-500ug/day of lead). Data such as those previously
presented (Section V - Sources of Lead Exposure Among the General Population)
suggest that increased air lead exposures in urban communities are
contributing to the extent of excessive lead exposures among urban adults as
summarized in Table VI-1. Since over 90% of airborne lead is due to lead
2
automotive emissions, these emissions are believed to be contributing
significantly to this problem.
Extrapolation from the evidence in Table VI-1 indicates that
approximately 1-2% of adult females and 3-5% of adult males residing in
urban areas have abnormally elevated blood leads (40ug/100g and above).
This observation reflects the probable existence of excessive lead expo-
sures among millions of urban adults. In selected sub-groups such as
-------
VI-2
garage mechanics and parking attendants, this proportion is markedly higher,
approaching 50% and above. Although these exposures are occupationally
related and could possibly be controlled by better industrial hygiene
practices, the source of lead is primarily from gasoline containing lead
additives.
Within each city in Table VI-1 the percentages of individuals with
abnormally elevated blood leads are generally consistent with the expected
gradients according to exposure category. However, especially when specific
exposure categories are compared from city to city inconsistencies become
evident. This may reflect exposure to different levels of atmospheric lead
3
in combination with differing amounts from dietary lead sources.
Table VI-2 summarizes existing data which demonstrate that abnormally
elevated blood lead levels among adults are found predominantly in urban
areas where greater exposures to airborne lead are more likely to occur.
When considering the data in this table, one must be aware that populations
being compared may not be appropriately matched for all of the pertinent
covariates recognized to influence blood lead levels. The people in the
individual geographic areas which were combined in this first comparison
were all women who were not always equally matched with respect to age,
smoking habits, and dietary lead exposures. However, consistent urban-
suburban differences for both smokers and non-smokers with higher blood
4
lead levels recorded in urban areas were found in each area. Since specific
urban-suburban comparisons also tend to minimize dietary differences, this
first comparison seems reasonably valid. (Individual urban-suburban
breakdowns were previously presented in.Table V-l).
-------
VI-3
The validity of the second and third comparisons are somewhat more
suspect than the first. In the second comparison the large differences
in numbers studied might in theory be important since, if only one
additional person in the suburban group were studied who happened to have
a blood lead level of 40ug/100g or above, the frequency of this occurrence
would have been approximately equal in both groups. However, the fact that
only 13% of the suburban group studied had blood leads of 20ug/100g or more
compared to 23% of the urban residents, suggests that a real difference
existed between the groups. The third comparison is least reliable since
many individuals of unknown history and residence are combined in this
instance; nevertheless there was a definite increase in the blood leads
from the urban when compared to the suburban category.
Among children, extensive surveys (see Table VI-3) have demonstrated
that excessive lead exposures have approached what many consider an
"epidemic" proportion. Approximately one quarter of the children tested
showed elevated blood leads of 40ug/100g and above. Although these
excessively exposed children are often residents of homes coated with lead
based paints, lead in the air, and consequently lead in dust and dirt may be
contributing to and aggravating this problem. For example, in some of
the children a history of exposure to lead based paint cannot be elicited
and housing investigations fail to reveal the presence of peeling lead
based paint (traditionally defined as paint containing 1% lead or greater).
In such cases other potential sources of lead exposure such as lead from
the air and lead which settles out from the air to contaminate dirt and
-------
VI-4
dust must be considered as possible contributing causes. This is discussed
in more detail in the previous section.
Recent preliminary data indicate that excessive lead exposure may
already be occurring before birth among babies born to mothers living
in urban environments. This is based upon reported umbilical cord blood
lead levels of 30ug/100g and above in these newborns. This is not much
below the levels at which clinical symptoms of lead poisoning in children
have been observed. Increased exposures to airborne lead in these urban
environments should be considered a possible factor contributing to this
problem. In Boston, where excessive drinking water contamination by lead
is recognized, one might also suspect this source to be a potential contri-
butor. For example, in a study conducted in the Boston area, umbilical
cord blood lead values of 30ug/100g or above were present in 3 of 13 (23%) of
5
babies tested who were born to urban mothers. Cord blood leads of 37 and
39ug/100 were observed in two of these babies, but cord bloods of 30ug/100g
and above were not found among any of the suburban babies studied. Since
less than 23% of mothers in urban areas are believed to have blood leads
of 30ug/100g or more, the Boston study probably reflects the role played
by lead in water as well as lead in air.
A second study examined umbilical cord blood lead levels among
babies born to mothers living only in New York City. Of 100 urban
newborns sampled, 6 were found to have umbilical cord blood lead levels
in the range of 25-34 ug/lOOg. This is reasonably consistent with the
reported occurrence of blood lead levels in this range among women residing
in New York City (see Table V-l). Several of these babies were probably
-------
VI-5
born with cord blood leads of 30ug/100g or above, again a level considered
to be evidence of excessive exposure.
A third study failed to demonstrate any difference in umbilical
cord blood lead levels between babies born to mothers living in urban
7
compared to suburban environments. Since only a small number of babies
were sampled (24 in total) this minimized the chances of detecting a
significant difference between the groups, should a real difference have
existed.
The relationship between blood leads in mothers and those in their
newborn babies as measured via umbilical cord sampling would be expected
to be dependent upon lead exposures to the mother. Findings such as these
above confirm what has already been well established, that lead can readily
cross the placenta from the mother to the baby. Possible concentration of
lead by fetal blood compared to maternal blood has also been reported which
may be of potential significance with regard to what is considered a safe
Q
blood lead level in an expectant mother.
In summary, considered as a group, there studies indicate the
probable existence of abnormally elevated umbilical cord blood lead
levels among babies born in urban environments. If these studies are at
all applicable to the general urban population, then significant percentages
of babies born in urban environments are probably exposed to excessive
amounts of lead even before birth.
-------
VI-6
TABLE VI - 1
Extent of Abnormally Elevated Blood Leads
City
Cincinnati
Los Angeles
Area
Oakland
Among Urban Adults
Exposure Category
Post Office Employees
Firemen
Service Station Attendants
Police1
Drivers of Cars
Parking Attendants
Garage Mechanics
L.A. Police1
Pasadena Male City Employees
L. A. Female Aircraft Employees
General L.A. Clinic Population5
L.A. Male Aircraft Employees^-
Female Clinic Patients5
Male Clinic Patients5
Philadelphia
Male Commuters 1
Police1
Downtown Male Residents
Number
Studied
140
191
130
40
59
48
152
155
88
87
45
291
53
36
43
113
66
Camden, Women Living Near Freeways 55
New Jersey
Composite Females from New York, Phila., 423
Urban and Chicago^
Samples Males and Females from 6 Cities 833
% of Blood Leads Equal
to or Greater than
40ug/100g
2.9
3.0
12.3
12.5
15.0
44.0
67.0
0.6
3.3
3.3
4.4
5.2
1.9
5.5
2.3
3.5
4.5
1.8
0.7
2.7*
* Only those above 40.
-------
VI-7
REFERENCES TO TABLE VI-1
1
"Survey of Lead in the Atmosphere of Three Urban Communities,"
Public Health Service Publication No. 999-AP-12.
2
Tepper, L.: "A Survey of Air and Population Lead Levels in Selected
American Communities" (7 City Study), Testimony presented at EPA
Public Hearing in Los Angeles May 3, 1972, and report submitted to
EPA, June, 1972.
3
Hofreuter, D. H., et al: "The Public Health Significance of Atmospheric
Lead," Arch. Env. Health 3:82-88, Nov 1961.
4
Daines, R. H. et al: "Air Levels of Lead Inside and Outside Homes,"
Ind. Med. Journal, 41: pp 26-28, Oct. 1972.
5
Goldsmith, J., California Department of Public Health, Testimony
Submitted to EPA July 11, 1972.
-------
VI-8
TABLE VI-2
Urban—Suburban Blood Lead Comparisons
in Adults
Group Studied
Number Studied
% Blood Leads Equal to or
Greater than 40ug/100g
Urban Females
Suburban Females
Philadelphia Males1
Urban
Suburban
Composite-'
Urban
Suburban
423
556
66
23
833
162
0.7
0
4.5
0
2.7*
0
*0nly those above 40.
-------
VI-9
REFERENCES TO TABLE VI-2
1
"Survey of Lead in the Atmosphere of Three Urban Communities,"
Public Health Service Publication No. 999-AP-12.
2
Tepper, Lloyd: "A Survey of Air and Population Lead Levels in Selected
American Communities," (7 City Study), Testimony presented at EPA
Public Hearing in Los Angeles May 3, 1972, and report submitted to EPA,
June, 1972.
3
Hofreuter, D. H., et at: "The Public Health Significance of Atmospheric
Lead," Arch. Env. Health 3:82-88, Nov. 1961.
-------
VI-10
TABLE VI- 3
Percentages
City
Baltimore1
Chicago1
New Haven1
Newark1
New York1
New York2
Philadelphia1
Washington1
Many Cities3
Aurora, 111.
Springfield, 111.*
Peoria, 111.4
E. St. Louis, 1114
Decatur, 111.4
Joliet, 111.4
Rock Island, 1114
E. Moline, 111.4
Robbins, 111.
Harvey, 111.4
Carbondale, 111.*
Norfolk, Va.4
New Haven, Conn
Washington, DC4
Rockford, 111.4
of Children
Years Tested
1968
1969
1970
1967-70
1969-70
1970
1969
1970
1971
1970
1970
1970
1971
1971
1971
1971
1971
1971
1971
1971
1971
1971
1971
1971
1971
NA
1971
NA
with Abnormally Elevated Blood Leads
Numbers Tested . % Blodd
Greater
665
746
939
120,000
1,897
594
2,648
84,368
81,626
3,496
808 (all ages)
1,152 (2 years)
2,309
449
670
387
376
793
383
285
298
103
226
264
1,225
1,339
1,821
1,200
Leads Equal to or
than 40ug/100g
25.3
27.9
31.5
20.0
29.8
38.9
45.5
28.7
20.2
34.0
5.8
22.0
9.1
24.3
30.1
31.3
24.7
12.2
24.3
21.1
11.4
12.6
16.4 '
17.0
22.7
23.7
39.2
19.5
-------
VI-II
REFERENCES TO TABLE VI-3
1
Lin-Fu, Jane S.: "Undue Absorption of Lead Among Children - A
New Look at an Old Problem," New Eng J of Med, Vol 286, pp 702-710, 1972,
2
Guinee, Vincent F.: "Lead Poisoning,"" American Journal of
Medicine, 52:283-288.
3
Challop, R. S., and McCabe, E. B.: "Childhood Lead Poisoning: A
Thirty City Neighborhood Survey," BCEM, USDHEW, May 23, 1972.
"National Estimates of Lead Based Paint Poisoning of Children,"
National Bureau of Standards Report 10651, Dec. 7, 1971 and Fine, P. R.,
Thomas, C. W., Suhs, R. H., Cohnberg, R. E. and Flashner, B. A.,
"Pediatric Blood Lead Levels, A Study in 14 Illinois Cities of
Intermediate Population," JAMA 221: pp 1479, Sept. 1972.
-------
VI-12
REFERENCES FOR SECTION VI - EXTENT OF ABNORMAL LEAD
EXPOSURES IN THE GENERAL POPULATION
1
"Airborne Lead in Perspective," National Academy of Sciences,
Washington, D. C., 1972, pp. 45 and 50.
2
Office of Air Programs Data File of Nationwide Emissions, 1970.
EPA, Research Triangle Park, N. C., July 1972.
3
Tepper, Lloyd: Testimony presented to EPA at Los Angeles Public
Hearing, May 3, 1972 and report submitted to EPA, June 1972.
4
Tepper. Lloyd and Levin, Linda: "A Survey of Air and Population
Lead Levels in Selected American Communities," Report Submitted to EPA
June 1972.
5
Scanlon, John: "Umbilical Cord Blood Lead Concentrations,"
Amer J Dis Child, 121:325-326, 1971.
6
Rajegowda, B. K., Glass, L. and Evans, H. E.: "Lead Concentrations
in the Newborn Infant," Journal of Pediatrics, 80:116-118, January 1972.
7
Harris, Paul: "Lead Levels in Cord Blood," Journal of Pediatrics,
80:606-608, April 1972.
8
Finklea, J. F.; Creason, J. C.; et al: "Transplacental Transfer
of Toxic Metals," Presented before Subcommittee on Toxicology of Metals,
Permanent Commisssion and International Association on Occupational
Health, Buenos Aires, Argentina, September 1972.
-------
VII. FINDINGS AND RECOMMENDATIONS
Findings
1. Lead is a known toxic substance for which no beneficial biological
role has yet been demonstrated.
2. Experimental evidence suggests that the least measurable quantities
of lead within cells are capable of affecting cellular metabolism and that
these effects are a function of lead concentration. For example, inhibition
of the enzyme delta aminolevulinic acid dehydrase in the peripheral blood
of man is a function of blood lead concentration even at blood lead levels
well below those generally considered excessive (40ug/100g and above).
Inhibition of this enzyme is not believed to be physiologically significant
until blood leads have reached 40ug/100g. However, this effect has been
noted in children as well as adults, although its true significance is at
present unknown. Since ALAD inhibition by lead in peripheral blood of
suckling rats correlates well with ALAD inhibition in the brains of these
animals, this suggests that a similar phenomenon might also occur in young
children. Recent associations of behavioral disturbances among children
with increased lead exposure, but at blood lead levels presently not
believed excessive (below 40ug/100g), raises the question whether lead
inhibition of enzymes in the central nervous system of children might be a
possible contributing factor in the etiology of these disturbances.
3. Susceptibility to lead may possibly be increased among young
children as compared to adults. New born babies conceivably are potentially
most vulnerable to lead. Exposure of the developing central nervous
system in utero, to lead, an established neurotoxic agent, should be
-------
VII-2
kept at a minimum. The conservative position favors a reasonable safety
factor between what is considered a safe blood lead level in children
and what is considered an acceptable exposure among the newborn.
4. Considerable difficulty exists in defining a single safe blood
lead level protective of everyone in the population. Variable respon-
siveness to lead probably exists among different age groups and even
within age categories. In this context, available scientific evidence
supports the following guidelines defining excessive lead exposures.
Blood lead levels above these guidelines in individuals do not necessarily
indicate that clinical disease is actually present. These guidelines
reflect a judgmental decision with regard to which levels of lead
exposure may be associated with a greater possible occurrence of adverse
clinical and/or subclinical effects.
a. Blood lead levels of 40ug/10Qg or above in adults are
considered evidence of excessive lead exposure.
b. For expectant mothers the upper acceptable blood lead
level should probably be no more than 30ug/100g. Low calcium diets have
been shown in experimental situations to increase gastrointestinal lead
absorption as well as lead storage in the soft tissues. Since there is
a requirement for more calcium than usual during pregnancy, this factor
may be important with respect to determining acceptable lead exposures
for expectant mothers.
c. A safe blood lead level protective of all children is no
more than 40ug/100g.
-------
VII-3
/-
d. Blood lead levels of 30ug/100g or above in newborn babies
obtained from umbilical cord blood should be considered evidence that
excessive lead exposure has probably occurred to the fetus in utero.
5. Though food and water usually account for more lead exposure
than airborne lead among the general population, airborne lead levels
3
around 2ug/m have been demonstrated to contribute to blood leads in
adults. These same air levels are associated with blood lead elevations
in children perhaps reflecting the dustfall lead exposure mechanism.
6. Though lead paint is considered to be the prime causal factor
in childhood lead poisoning, other environmental sources such as air lead
and lead which settles out from the air to contaminate dirt and dust are
also capable of contributing to this problem. Large percentages of children
are known to ingest non-food objects including dirt and dust. For these
children, possible ingestion of lead contaminated dirt and dust should be
viewed as potentially harmful.
7. Levels of lead in street dirt and house dust in urban areas
have been found to be far greater than those considered safe in paint by
the Food and Drug Administration. Evidence exists to indicate that the
presence of lead in gasoline contributes to high levels of lead in dust
and dirt found in areas and homes which are located near busy roadways.
8. Individuals within groups may often be excessively exposed to
lead even though average lead exposures for the group are well within
normal limits. On this basis, although average blood lead levels among
urban populations are well within normal limits, considerable numbers of
-------
VII-4
individual urban residents are found to have blood lead levels exceeding
40ug/100g.
a. Small increases in average blood lead levels found among
adult residents in urban compared to suburban areas may well account for
the relatively large number of individual urban adults found to be
excessively exposed to lead. Recent surveys of adult populations indicate
that approximately 1-2% of urban females and 3-5% of urban males probably
have blood lead levels of 40ug/100g and above. Residence in areas
where air lead levels are greatest is consistently associated with this
finding. Approximately 5-10% of women residing in urban areas have blood
lead levels of 30ug/100g and above, a level which in expectant mothers
should be considered a potential hazard to newborn babies.
b. Excessive lead exposures among children have approached what
many consider an "epidemic" proportion. Extensive surveys involving over
one quarter of a million children, document that approximately 25% of
children tested have abnormally elevated blood leads of 40ug/100g and
above. Although these adversely affected children are often residents
of homes coated with lead based paints, lead in the air and consequently
in the dust and dirt present additional sources of exposure which may
contribute to and aggravate this problem.
c. Recent preliminary data suggest that excessive lead exposure
may already be occurring before birth among babies born to mothers
living in urban environments. Significant numbers of babies born in the
central city may have umbilical cord blood lead levels well above 30ug/100g,
and even approaching 40ug/100g, a level close to those at which clinical
symptoms of lead poisoning in children have been observed. Exposure of
-------
VII-5
expectant mothers to airborne lead in urban environments could be an
important factor contributing to these blood lead elevations.
9. Over 90% of airborne lead emissions are. a result of combustion
of gasoline containing lead additives.
Recommendations
These results cast doubt on the adequacy of the previous position
taken by EPA that achievement of a 2ug/m air lead goal would assure a
reasonably complete degree of public health protection. This is
especially true in view of the possibility (a) that blood lead levels
at or above 30ug/100g in mothers might contribute to similar blood lead
levels among their newborn babies and (b) that air lead levels around
2ug/m may be associated with potentially harmful levels of lead in
3
dirt and dust. On this basis, further air lead reductions below 2ug/m
would seem indicated.
Though none of the above findings viewed individually and in the
context of possible experimental error can be taken as conclusive
evidence that airborne lead by itself is a current public health problem,
considered together, they do suggest that airborne lead is contributing to
excessive total lead exposures among the general urban population. Every
effort should, therefore, be made to reduce all preventable lead exposures,
including airborne lead, to the fullest extent possible.
-------
APPENDIX A - OVERVIEW OF EPA'S CONCLUSIONS REGARDING RESPONSES RECEIVED
TO QUESTIONS WHICH APPEARED IN THE FEDERAL REGISTER
(Vol. 37, No. V15, pp. 11786-11787, June 14, 1972)
Question 1: In the light of any criticisms you may have of the
Goldsmith-Hexter approach and the Environmental Protection Agency's use
of a regression equation based upon it (see Figure 3-3 of "Airborne Lead
in Perspective," National Academy of Sciences, 1972; and Table 7 of "Health
Hazards of Lead," Environmental Protection Agency, revised April 11, 1972,
which was corrected in "Corrections and Additions to Health Hazards of Lead,"
April 27, 1972), what are the permissible uses and limitations in its
application for obtaining reasonable estimates of blood lead levels as a
function of air lead exposures?
The Goldsmith-Hexter regression equation relates changes in the
average blood lead level of various groups to corresponding changes in
their exposure to atmospheric lead. EPA believes that the physiologic
basis behind the Goldsmith-Hexter approach is correct; that is, at higher
atmospheric lead exposures blood leads will increase. The major problem
with this approach has been the difficulty correlating blood lead levels
3
with air lead at low air lead exposures (below 2ug/m ). At these low air
lead levels, the normal lead intake from food and water is greater than
that from air, but not so great that air lead exposures do not affect blood
lead levels. Hence even small variations in dietary lead intake which
1
ranges from 100-500 ug per day will tend to mask any changes in blood
lead due to variations in air lead exposure. Unless dietary lead exposure
can be kept reasonably constant, the likelihood of observing a correlation
between blood lead and air lead at low air lead concentrations is very slim.
-------
A-2
2
In judging the validity of the Goldsmith-Hexter regression equation
for relating blood lead levels to air lead exposures several important
factors must be kept in mind. All data used in this regression analysis
were not always ideally suited for this purpose. Air lead exposures were
at times estimated rather than measured and blood leads were not always
determined at appropriate points in time in relation to air lead measure-
ments which were made. Further, differences in dietary lead intake may
have confounded blood lead differences among groups used in the regression
analysis. Finally, average blood lead levels for the groups were compared
under circumstances which were not justified since the groups were often of
different size with unequal variances. Use of only average blood lead
levels also tends to obscure a considerable quantity of useful information
present in the original data, such as the occurrence of abnormally elevated
blood leads.
Primarily for the above reasons, EPA does not believe that use of
2
the specific regression curve developed by Goldsmith and Hexter is the
optimal approach for predicting general population responses to air lead
exposures. Reluctance to use this particular approach in no way implies
that the Goldsmith-Hexter equation was not valuable. If anything, it
highlights the importance of considering the role played by airborne lead
as a determinant of blood lead level.
EPA's reluctance to employ this equation in a quantitative way is
a result of uncertainty as to its preciseness for describing responses of
blood lead to air lead especially at low air lead exposures. Our decision
not to employ this equation does not mean that EPA does not consider air
-------
A-3
lead to be an important exposure mechanism in the general population.
Additional methods of statistical analyses focusing upon individual rather
than average blood leads demonstrate that airborne lead is a significant
factor contributing to blood lead. One noted biostatistician in commenting
3
upon the Goldsmith-Hexter regression equation concludes:
"It is interesting to note that all of the variations in fitted
trend lines that have been suggested would indicate that there is
some increase of average blood lead as air lead increases at any
level of air lead. The various curves differ with regard to the
rate of this increase, but the data certainly do not encourage
the notion of a threshold below which changes in air lead are
unrelated to blood lead... it would seem to be highly imprudent,
with our current information, to assume that there is any safe
threshold below which air lead does not affect blood lead."
Comments received by EPA in response to this question have generally
supported our reconsidered position that use of the Goldsmith-Hexter
equation in a quantitative way to predict population responses to air lead
exposures is not the ideal approach.
4
For example, a recently completed study by DuPont which measured
blood leads in various occupational groups using personal air lead sampling
devices capable of measuring individual air lead exposure comes to a similar
conclusion:
"Any attempt to predict blood lead levels solely on the use of the
average relationship line developed in this study (which is similar
-------
A-4
to the Goldsmith-Hexter approach as well as the "7 City Study"
approach) could be misleading because the effect of lead intake
from other sources such as food and drink is significant."
Several prominent biostatisticians also concur with EPA's preference
to consider individual blood lead values as well as average blood leads
when comparing responses of groups exposed to various air lead levels.
For example, according to Dr. Enterline:
"...A test of statistical significance of these data (data used
in Goldsmith-Hexter regression equation) is difficult to
interpret, however, since what must be of interest is the
relationship between air lead levels and individual blood lead
5
levels...not means or groups of people."
Dr. Robert Reed, Chairman of the Department of Biostatistics at the
Harvard School of Public Health is in agreement with this approach:
"A trend line is essentially an average relationship between
air and blood lead. From the public health point of view, we
must be concerned with individual variation in blood levels.
It is almost inevitable that at ambient air levels which produce
borderline 'acceptable1 blood levels there will be an important
fraction of the population with higher 'unacceptable1 blood
levels. This variation may be due to a number of factors.
An important aspect of this issue is the possibility of a serious
additive effect of air-lead and dust-lead from air to the lead
paint exposure of children in certain central city areas."
-------
A-5
REFERENCES FOR APPENDIX A - Question 1
1
"Airborne Lead in Perspective" National Academy of Sciences,
Washington, D.C. 1972, p 50.
2
Goldsmith, J. R. and Hexter, A. C., "Respiratory Exposure to
Lead: Epidemiological and Experimental Dose - Response Relationships,"
Science, 158:132-134, 1967.
3
Reed, Robert, Professor of Biostatistics, Harvard School of
Public Health, Testimony submitted to EPA, August 4, 1972.
4
Supplemental Statement by E. I. DuPont De Nemours & Company,
Inc. Relative to EPA's Request for Additional Information on the
Health Effects of Airborne Lead, July 12, 1972, Section 6, "Relationship
of Airborne Lead and Indices of Lead Absorption" presented at the
International Symposium on Environmental Health Aspects of Lead,
Amsterdam, October 2-6, 1972.
5
Cole, Jerome, Testimony presented at Dallas Public Hearings,
p. 459 of Hearing Record, April 28, 1972.
6
Reed, Robert, Testimony Submitted to EPA, August 4, 1972.
-------
A-6
Question 2: How accurate a reflection is blood lead of lead body burden?
What is the effect of elevated blood leads upon lead body burden? Can
small increments in blood lead be expected to result in a significant lead
body burden elevation? From a public health point of view, is it permis-
sible to allow slight increases in lead body burdens among the general
population when this increment can be prevented? Can the pool of body
lead stored in the bone be viewed as totally "physiologically inert"?
It is known that chelation therapy of children with elevated blood leads
can result in acute clinical symptoms of lead poisoning as a result if
mobilizing lead from bone. Is there any evidence that subtle metabolic
changes could also mobilize this lead pool under other conditions?
EPA's position after having reviewed the responses received to this
question is that there is no simple answer regarding any of these issues.
Whether blood lead is in all instances an accurate reflection of lead
body burden is difficult to say. Blood lead appears to be a reasonable
indicator of recent lead exposure. Certainly the majority of available
evidence regarding adverse clinical and/or subclinical effects of lead
is related to blood lead measurements as an index of either body burden
or recent exposure. Two lead additive manufacturers support the use of
1,2
blood lead as a reasonable indicator of lead body burden. Traditional
use of blood lead as an exposure index in occupational situations and the
correlation of biological effects with blood lead support the continued
utility of blood lead determinations as indices of both recent exposure
3
and body burden.
-------
A-7
Whether small increments in blood lead can be expected to result
in significant lead body burden elevations is a complex problem. One
manufacturer of gasoline lead additives feels that any significant
sustained increase in lead exposure will produce increments in lead
4
body burden. The prime difficulty centers around how much of an increase
in lead exposure is required before definite increases in lead body
burden occur. Most of the body's lead content (90-95%) is stored in
bone. Hence slight increases in blood lead level may not raise total body
burden per se, but may still pose a health hazard in terms of additional
lead available for storage in soft tissues including the central nervous
system. Further, mobilization of even a small portion of lead from bone
into the soft tissues could pose a definite threat to health.
After reviewing the evidence EPA concludes that while most lead
stored in bone is probably not generally available for mobilization, '
under certain instances, expecially rapid physiologic alterations, lead
from bone may well be mobilized into the soft tissues. Conditions such
as pregnancy, and/or any intercurrent illness which cause demineralization
of bone could result in mobilization of lead from bone,'which in some
instances could be hazardous.
Although several investigators have tried unsuccessfully to mobilize
lead from bone under experimental conditions, this does not constitute
proof that under all conditions lead stored in bone is in fact physio-
Q
logically inert. Recent evidence suggests that lead stored in bone may,
q
in fact, inhibit hemoglobin synthesis in the intact animal.
-------
A-8
Studies involving the possible effect of dietary deficiency on lead
metabolism indicate that low calcium diets may significantly change the
partition between the amount of lead stored in bone and that stored in the
soft tissues with more lead being found in soft tissues compared to bone
under these conditions. On this basis, calcium deficient diets may
possibly result in the mobilization of lead from bone. Since relatively
more calcium is required during pregnancy, this physiologic state might
predispose to a similar mobilization of lead from bone.
Dr. Laurence Finberg, a member of the American Academy of Pediatrics,
Committee on Environmental Hazards, is in general agreement with EPA's
position and notes:
"I am quite sure that the pool of lead in the skeleton is
not physiologically inert under all circumstances. A number
of metabolic events which affect hydrogen ion or divalent
ion metabolism will affect the lead pool. Since lead does
not appear to have any necessary role in life processes,
its presence may be looked upon as the biologic equivalent
of a loose monkey wrench in the machinery."
-------
A-9
REFERENCES FOR APPENDIX A - QUESTION 2
"Comments of Ethyl Corporation on EPA's Proposed Lead Regulations,"
July 13, 1972.
2
"Supplemental Statement by E. I. DuPont De Nemours & Company, Inc.
Relative to EPA's Request for Additional Information on the Health Effects
of Airborne Lead," July 12, 1972.
Hammond,. Paul B., Testimony submitted to EPA, June 8, 1972; and
Goldsmith, John, Testimony submitted to EPA, July 11, 1972.
4
"Comments of Ethyl Corporation on EPA's Proposed Lead Regulations,"
July 13, 1972, p. 11.
5
Calandra, J. C., Testimony submitted to EPA, July 14, 1972.
Barry, P. S. I. and Mossman, D. B., "Lead Concentrations in Human
Tissues," Brit J Indust Med 27:339-351, 1970.
7 Goldsmith, John, Testimony submitted to EPA, July 11, 1972.
Q
Hammond, Paul, Testimony submitted to EPA, June 8, 1972.
q
Kahn, Ephraim, Testimony presented at L.A. Public Hearing,
May 2-4, 1972, p. 163 of Hearing Record.
10 Goyer, R. A., and Mahaffey, K.R., "Susceptibility to Lead Toxicity,"
Env. Health Pers;. Exp. Issue No. 2, Oct. 1972.
Finberg, Laurence, Testimony submitted to EPA, June 20, 1972.
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A-10
Question 3: The Environmental Protection Agency has relied upon the
National Academy of Sciences' Report (Appendix C. p. 249, footnote "A")
for estimates of daily respired air by an average adult in its own cal-
culations in Table 7 of the "Health Hazards of Lead" paper. How accurate are
these estimates of pulmonary physiology (a) that an adult male breathes
23 cubic meters of air per day, (b) that 30% of respired lead particles
will be retained, and (c) that nearly 100% of retained lead particles
will be absorbed? Is there additional evidence available in this area
besides that which is cited in the NAS Report?
The wide variance of opinion received in reply to this question
emphasizes the importance of considering the entire spectrum of biological
response to lead that exists in the general population. The real world
is simply not adequately described in terms of only the average response.
For example, estimates of daily ventilatory volume can be developed
by extrapolating from metabolic oxygen requirements. On this basis a figure
of 23 cubic meters per day as an average daily respiratory volume is too
high. Even considering the wide spectrum of metabolic requirements within
the population, a more reasonable estimate would be in the range of 13-20
1
cubic meters per day. Dr. Goldsmith from the California State Department
3 3
of Health also feels that the 23m figure is too high and that 15-20m
2
is probably a better estimate.
On the other hand, Dr. Paul Hammond, Chairman of the National Academy
of Sciences Lead Panel which wrote "Airborne Lead in Persepective" considers
3
the 23m figure to be acceptable. An International Council on Radiation
-------
A-n
Protection report (still in draft stage) recommends 23 cubic meters as
3
an appropriate estimate for average daily respiratory volume. Dr..
J. C. Calandra of Northwestern University and Medical Director of the
Houston and NALCO Chemical Companies, however, critizes the basis upon
4
which the ICRP arrived at this figure.
A similar difference of opinion exists with regard to how much inhaled
lead is ultimately retained in the lung. The National Academy of Sciences'
Report on lead concluded that 30-37% was a reasonable figure for pulmonary
5
lead deposition. Dr. Paul Hammond believes this figure to be based upon
sound scientific evidence; Dr. Calandra, however, considers that
available evidence supports a much lower figure.
Disagreement also exists with respect to how extensively particles
which have been retained in the lungs will actually be absorbed into the
blood stream. A report of the National Academy of Sciences concluded that
o
virtually all lead deposited in the lung is retained. All this lead is
probably ultimately absorbed into the blood stream.
A task group on lung dynamics of the ICRP considers a figure of
17-18% to more closely describe total blood absorption related to
respiratory lead inhalation including factors for both particle retention
9
and ultimate absorption of retained particles. Other medical opinions
consider this overall absorption figure to be even lower. Dr. P.
Lawther sums the situation up this way:
"It would appear that little of the speculation on the uptake of
lead inhaled in the form of aerosols in the exhaust from petrol
-------
A-12
engines is based on solid and established fact... In the absence of
such data, the only evidence relating to the effect of these
exhaust gases is from epidemiological studies on man."
Hence, EPA concludes that the entire adult population cannot be well
characterized in terms of simple average physiologic parameters. A range
of responses is a much more reliable reflection of the real world. On
this basis, EPA feels that available evidence supports 13-23 cubic meters
per day as the range for ventilatory volume in the general adult population
and 17-30% as the overall range for absorption of lead particles in the
lung, including factors for pulmonary deposition as well as absorption
of these retained particles. Ultimately, however, epidemiologic studies
provide the best evidence regarding effects of automotive lead emissions
upon man.
-------
A-13
REFERENCES FOR APPENDIX A - QUESTION 3
1
Earle, Richard, Testimony presented at EPA Public Hearing, Dallas,
Texas, p. 277 of Hearing Record, April 28, 1972.
2
Goldsmith, John, Testimony submitted to EPA, July 11, 1972.
3
Hammond, Paul, Testimony submitted to EPA, June 8, 1972.
4
Calandra, J. C., Testimony submitted to EPA, July 14, 1972,
pp. 8-11.
5
"Airborne Lead in Perspective" National Academy of Sciences;
Washington, D. C., 1972 pp. 57 & 66.
6
Hammond, Paul, Testimony submitted to EPA, June 8, 1972.
Calandra, J. C., Testimony submitted to EPA, Table 1, May 19, 1972.
8
"Airborne Lead in Perspective, " National Academy of Sciences,
Washington, D. C., 1972, p. 62.
9
Cole, Jerome, Testimony presented at Dallas Public Hearing, p. 455 of
Hearing Record, April 28, 1972.
10
Calandra, J. C., Testimony submitted to EPA, July 14, 1972.
11
Lawther, P. et al "Airborne Lead and its Uptake by Inhalation,"
Lead in the Environment, Proceedings of a conference held at the
Zoological Society of London, pp. 8-28, January 27, 1972.
-------
A-14
Question 4: What is an appropriate safety factor for extrapolating
industrial threshold limit values (TLV) to the general population?
Should such an extrapolation to the general population even be permitted?
The proposed TLV for lead is due to be revised to 150ug/m for a 40 hour
week. On a weekly basis this corresponds to breathing air continually
3
at between 35-40 ug/m of lead. If TLV's can be extrapolated to the
general population, what would be an appropriate safety factor for this
purpose so that all groups, including those most susceptible to lead,
will be protected?
A review of the evidence presented does not support extrapolation of
industrial threshold limit values to the general population. Such extra-
polation would not assure protection of those groups within the general
population who are most susceptible to lead.
When extrapolating from occupational to general population situations,
the following factors must be considered: (1) the wider variation of age
in the general population compared to the occupational population. In-
cluded in the general population are the very young and the very old, pre-
cisely those who are almost always most susceptible to pollution in any
form; (2) the physical health of occupational workers. Those in occupations
tend to be healthier and hence less susceptible to pollution than those in
the general population. Occupational groups, for example, do not usually
include those with chronic diseases; (3) occupational groups receive pre-
employment medical examinations to exclude those highly susceptible
individuals—people exposed in the general population are not so excluded;
and (4) occupational groups receive periodic medical examinations while
on the job to detect early disease changes. This opportunity is not
always available to those exposed in the general population.
-------
A-15
A British industrial health physician noted that in over 10 years of
industrial lead health experience, he had performed some 50,000 medical
examinations covering 8,000 man-years of risk. This corresponds to an
average of over 6 medical exams per man per year and reflects the potential
gravity of the situation with respect to increased lead exposure. The
general population is not afforded the opportunity for this close medical
supervision to detect effects associated with excessive exposures to lead.
Numerous authorities on lead support EPA's position that extrapolation
of industrial lead standards to the general population cannot be justified.
For example, Drs. T.J. Chow, of the Scripps Institute of Oceanography and
a consultant to the National Academy of Sciences' lead panel, and Claire
Patterson, of the California Institute of Technology, feel that industrial
threshold limit values are not based upon valid scientific data and
2
eventually will be shown to be harmful. Dr. John Goldsmith, an authority
on general population as well as industrial lead exposure, believes that
extrapolation of threshold limit values to the general population is
inappropriate, especially for children. Dr. Finberg, a member of the
American Academy of Pediatrics Committee on Environmental Hazards has
written:
"I would think, emphatically, that it is not safe to
extrapolate industrial threshold limit values to the
general population. For example, the general popula-
tion has in it pregnant women with their developing
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A-16
fetuses. It also has young children and many sick
people, including those with cerebral vascular disease."
Two leading manufacturers of lead additives are also in general
agreement that TLV's should not be extrapolated to the general population:
"There exists no factor that permits the simple
extrapolation of TLV values (established for the
5
industrial population) to the general population."
"Because of the wide differences between industrial
groups and the general population in exposure time,
the types of populations involved, and the opportunity
to monitor both health and exposure, it does not seem
appropriate to use TLV's as a basis for developing air
6
quality criteria."
Finally, the Department of Health, Education and Welfare is in agreement
with this position and concludes:
"We do not believe that the industrial threshold limit values
(TLV) should be extrapolated to the general population."
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A-17
REFERENCES FOR APPENDIX A - QUESTION 4
Williams, M. K., Testimony presented at EPA, Washington, D. C.,
Public Hearing, pp.342-355 of Hearing Record, April 12, 1972.
2
Patterson, C. C., and Chow, T. J., Testimony submitted to EPA,
July 6, 1972.
3
Goldsmith, John, Testimony submitted to EPA, June 11, 1972.
4
Finberg, L., Testimony submitted to EPA, June 20, 1972.
5
Comments of Ethyl Corporation on EPA's Proposed Lead Regulations,
p. 24, July 13, 1972.
DuPont, comments submitted to EPA, p.4, July 12, 1972.
Richardson, Elliot, Secretary, DHEW, letter to EPA Administrator
William D. Ruckelshaus, August 11, 1972.
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A-18
Questions 5 and 6:
5. In regard to the dustfall lead theory (p 139 of the NAS report): How
much of a hazard is dustfall lead to children prone to pica? The Environ-
mental Protection Agency's calculations indicate that continued ingestion
of even small amounts of lead contaminated dust and dirt containing as
much as 0.25-0.35 percent lead could theoretically result in dangerously
elevated blood leads among children, or could contribute significantly to
additional unnecessary lead burdens in children with other known lead
exposures (such as lead paint). Will the Environmental Protection Agency's
proposed 60-65 percent reduction of leaded automobile emissions signifi-
cantly reduce the risk of this potential contamination?
6. Although lead paint has traditionally been considered the prime
causal factor in childhood lead poisoning, how effective would reductions
in other known environmental sources of lead exposure (such as dustfall)
be in helping to reduce the risk of undue lead exposure among children
also exposed to peeling lead paint? How clear is it that all lead
poisoning in children is, in fact, caused only by lead paint? Since many
years are required to solve the lead paint problem, would the risk of
undue lead absorption and possible lead poisoning not be reduced by also
decreasing airborne lead and consequently lead in dust?
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A-19
EPA agrees that peeling lead based paint from dilapidated housing
is a problem. This Agency has supported HEW in its effort to reduce
the hazard associated with lead paint among future generations. The
main question is whether reductions in the use of gasoline lead additives
will also help to decrease the risk of not only lead poisoning but also
excessive lead exposure among children. Previous investigations of the
lead paint poisoning problem have not always considered the magnitude of
paint exposure with respect to other environmental lead sources which
may also be contributing to abnormally elevated blood leads. Clearly
blood lead is a function of all sources of lead exposure.
For example, a recent publication by Dr. Vincent Guinee, Chief of
2
the Lead Poisoning Control Bureau of New York City indicates that only
76.3% of children with lead poisoning lived in homes containing lead
paint (defined as paint containing 1% or more lead). Although on
reinspection of these homes additional peeling paint surfaces of 1% or
more lead will probably be found, this by itself does not completely put
this problem in true perspective. A considerable number of lead poison-
ing cases (for this purpose defined as blood leads of 60ug/100g or greater
in children) are associated with lead paint environments containing lead
paint predominantly at lead concentrations of 1% or below.
In testimony before the Senate Health Subcommittee, Dr. Guinee
presented the fact that of 418 samples of paint removed from broken
surfaces in 25 apartments where a lead poisoning case resided, nearly
two-thirds of these samples were found to contain lead paint at
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A-20
concentrations of 1% or less. Over half were found to contain lead
plaint Of 0.5% or less. Although the breakdown was not available with
respect to whether most of the samples containing markedly elevated
paint concentrations were predominantly found in a selected number of
homes, this is a reasonable possiblity. Accordingly, a considerable
number of lead poisoning cases are probably associated with home paint
environments containing predominantly paint of 1% lead or less. As
evidence of its concern for the potential harm caused by lead paint at
this concentration, the FDA has recently established 0.06% as what it
4
believes to be a safe level of lead in paint.
When this observation that excessive lead exposure is associated
with paint of 1% lead or below is put into the context of other environ-
mental lead exposures (including food, water, air, dust and dirt), the
potential contribution of these additional sources to the problem cannot
be ignored. Of these sources cited, lead content of food and water are
not at the moment always easily controlled. However, exposures through..
lead in air and consequently lead falling out from the air to contaminate
dust and dirt can be readily reduced. Further, exposures to airborne lead
as well as lead in dust and dirt must be considered additional burdens to
children already exposed to peeling lead based paint. These additional
factors may in part explain why such large numbers of urban children
have abnormally elevated blood leads.
One recent study designed to test the possible effect of these
additional factors upon blood lead supports this point of view. In
-------
A-21
this investigation, 230 rural children and 272 children from an urban
poverty area were examined for excessive lead exposure in the summer
of-1971. Nearly all of the rural children with excessive lead body
burdens lived in homes containing at least one surface with 1% lead
paint or greater. However, this paint hazard could be found on accessible
indoor and exterior surfaces in homes of only 60% of the urban children
found to have excessive lead exposure. These findings are consistent with
the position that excessive lead exposure of young children in urban areas
is caused not only by lead in paint, but also by lead in air, in dust,
and in dirt.
Evidence accumulated by the Environmental Protection Agency,6
indicates that dustfall lead and concentrations of lead in dustfall
generally..decrease with increased distance from roadways. Levels of lead
in dustfall of 0.3% were commonly found and levels of 0.5% or more were
observed.^ These findings suggest that vehicular lead emissions may be
contributing significantly to high concentrations of lead in dustfall
found in urban areas. Street dirt in urban areas has been documented
o q
to contain as much as 1% lead.0'
Elevated lead concentrations have also been found in dust collected
from indoor urban dwellings. Concentrations of lead in indoor dust in
central city areas averaging 0.2% are reported. Although lead from
peeling paint may have contributed in part to lead contaminated dusts
found in older homes collected as vacuum cleaner samples, this factor
was not a reasonable explanation for the often high dust lead values
found by this study in homes built in the 1950's and after. Airborne
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A-22
lead was felt to be a significant source of this lead contamination.
Lead in dustfall and consequently lead in street dirt are probably
related to the total quantity of automotive lead emissions, although
no simple relationship has been demonstrated between the quantity of lead
in the air and that in the dust. This in part may be explained by
settling of large lead particles deposited close to emission sources com-
pared to the movement of smaller respirable lead particles much farther
distances. Thus, it is difficult to relate specific levels of airborne
lead directly to levels of lead in dust. However, the role of automotive
lead emissions in contributing to urban lead fallout from the air has
been demonstrated. For example, average soil lead levels collected in
front yards of homes in urban areas are two to three times greater than
soil lead concentrations in back yards which are located further away
from roadways.l^ Automotive lead emissions are felt to contribute
significantly to this difference.
Precise information with respect to the gastrointestinal absorption
of lead contaminated dirt and dust relative to lead containing paint are
not presently available. However, cases of clinical lead poisoning or
excessive lead exposure among children known or suspected tp eat dirt,
but without known excessive lead exposure directly from paint, have been
reported.13,14
Demonstration of excessive lead exposures among children residing
near a lead smelter in El Paso, Texas, further emphasizes the importance
of the dustfall lead exposure mechanism. Information available to EPAl5
indicates that lead in paint could not have been a major factor in the
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A-23
etiology of these abnormally elevated blood lead levels found among
children residing near the lead smelter. Soil lead levels in the
vicinity of this smelter averaged 0.4%-0.5% lead with a range of 0.15%
to just over 1%. These average levels are not significantly different
from levels of lead in dirt and soils reported in many urban streets and
parks.
Though air lead levels were also significantly elevated near the
smelter, most of the airborne lead (approximately 75%) was judged to be
in the non-respirable range. The fact that a larger percentage of 1-5
year old children (89.2%) had abnormally elevated blood leads compared
to 6-17 year olds (64.7%) suggests that combined exposure to airborne
lead as well as ingestion of lead contaminated dusts was contributing
significantly to this problem in the group most likely to ingest non-food
items, the 1-5 year olds. Hence, levels of lead in street dirt of the
magnitude found near the smelter must be viewed as a potential hazard for
children with pica.
Many medical opinions submitted in testimony to EPA expressed
concern for this potential hazard. Dr. Finberg of the American Academy
of Pediatrics writes:
"The dustfall lead theory seems quite reasonable and I
believe that dustfall lead will represent a hazard to
some children. In our own clinical experience, we have
seen children who were dirt eaters with elevated blood
leads and signs of toxicity where we could not incrim-
inate painted surfaces in the household or other parts
of their environment."'"
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A-24
Dr. Paul Hammond, Chairman of the NAS Lead Panel notes:
"The lead panel of the NAS expressed no firm conviction
as to the actual contribution of dustfall to the total
lead input of young children. It definitely was concerned
that street dust might in some cases be a major contribu-
tor to the total lead assimilation of some children who
have been found to have blood lead concentrations of
40ug/100g. I do not think it is at all clear that all
childhood lead poisoning can be attributed to paint. The
relatively large number of city children with blood lead
levels in excess of 40ug/100g may or may not be attributed
to eating paint...street dust may well be a significant
source."
Dr. Anthony Mustalish of the New York City Department of Health
generally agrees:
"Although to my knowledge no cases of lead poisoning
have been attributed to atmospheric lead alone, there
is growing evidence that atmospheric lead contributes
to this body burden and in inner city children this
I Q
contribution may aggrevate an already compromised system; °
Finally, Elliot Richardson, Secretary of the Department of Health,
Education and Welfare, has written in a recent letter to EPA Administrator
William Ruckelshaus:
"For those children with pica who eat dirt, the danger
19
from exposure to lead containing dust and dirt is great."
-------
A-25
Although preliminary data failed to show any difference in blood
lead levels among groups of children residing in an area of high soil
lead content compared to those residing in a low soil lead area,^ EPA
does not believe that this study contradicts the potential importance
of the dustfall lead exposure mechanism. Levels of lead in soil were
not reported in a way to relate concentrations around the homes of
individual children to their specific blood lead levels. Further,
levels of lead were not measured in the housedust from homes in which
the children actually lived and the data available to EPA were not
broken down according to age so that blood leads in the youngest
children could be compared. Finally, the lead exposure gradients
between areas reported in this study were rather low with soil lead
concentrations averaging approximately 0.1% in the high exposure
area compared to 0.05% in the low exposure area. The high exposure
area was thus characterized by soil lead levels considerably less
than those reported to occur in street dirt, in soil and in dust
inside homes from several American cities where these data have been
collected.
In summary, EPA's position is rather straightforward. If paint
containing less than 1% lead can contribute significantly to abnormally
elevated blood leads and even to lead poisoning, then the potential
contribution to this problem of dust and dirt containing similar
quantities of lead cannot be ignored.
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A-26
Although lead paint and lead in dust and dirt may not always be
equally absorbed from the gastrointestinal tract, current levels of lead
in street dust and dirt are considerably higher than that recommended
as a safe level of lead in paint. Lead in dust and dirt would pose an
additional hazard to a child aready exposed to peeling lead based paint.
Reduction of airborne lead levels for purposes of decreasing the
concentration of lead found in urban dust and dirt would thus be a prudent
decision.
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A-27
REFERENCES FOR APPENDIX A - QUESTIONS 5 & 6
1
Bridbord, K.; Shy, C.; Hammer, D.; Goldberg, H.; Newill, V.;
and Nelson, W.: "A Control Strategy for Lead in Paint," Congressional
Record, Extension of Remarks, pp. E1010-E1011, February 9, 1972.
2
Guinee, Vincent, "Lead Poisoning," Am J Med 52:283-288, 1972.
3
Guinee, Vincent, "The Position of NYC on the Control of Childhood
Lead Paint Poisoning," Submitted to the Subcommittee on Health of the
Committee on Labor and Public Welfare, United States Senate, March 9,
1972.
4
DuVal, Merlin K., Assistant Secretry for Health and Scientific
Affairs, Department of Health, Education and Welfare, Testimony
before the Subcommittee on Health, Committee on Labor and Public Welfare
United States Senate, March 10, 1972.
5
Lepow, Martha L., Testimony before Subcommittee on the Environment,
Committee on Commerce, United States Senate, May 8, 1972.
6
Creason, J. P.; McNulty, 0.; Heiderscheit, L. T.; Swanson, D. H.;
and Buechley, R. W.: "Roadside Gradients in Atmospheric Concentrations
of Cadmium, Lead and Zinc," presented at the Proceedings of the Fifth
Annual Conference on Trace Substances in Environmental Health,
June 29-July 1, 1971, Columbia, Missouri.
7
Ibid.
8
Kreuger, Harold, Testimony presented to EPA, July 10, 1972.
9
Fritsh, Albert, and Prival, Michael, Center for Science in the
Public Interest, Testimony Presented to EPA, 1972.
10
Kreuger, Harold, Testimony presented to EPA, July 10, 1972.
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A-28
11
Creason, et al, op.cit.
12
Pinkerton, C., Hammer, D. I., Hinners, T. A., Kent, J. L.,
Hasselbad, V., Lagerwerff, J. V., and Ferrand, E. S., "Trace Metals in
Urban Soils and Housedust," paper presented to Environment Section,
APHA Centennial Convention, Atlantic City, New Jersey, Nov. 16, 1972.
13
Finberg, Laurence, Testimony present to EPA, June 20, 1972.
14
Lepow, Martha, Testimony before Senate Subcommittee on
Environment, May 9, 1972.
15
Chisolm, J. Julian, Letter to James M. Simpson, June 29, 1972.
16
Finberg, L., Testimony presented to EPA, June 20, 1972.
17
Hammond, Paul, Testimony submitted to EPA, June 8, 1972.
18
Mustalish, Anthony, Testimony presented at Washington, D. C.
Public Hearing, April 11, 1972.
19
Richardson, E., letter to EPA Administrator Ruckelshaus, dated
August 11, 1972.
20
Cole, Jerome, ILZRO, Testimony submitted to EPA, July 11, 1972.
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A-29
Question 7: What is the consequence upon the environment in general
of allowing large quantities of lead to be expelled into the atmosphere
from motor vehicle exhausts? Does this environmental contamination
pose any direct or indirect threat to man?
A concise answer addressing the problem of possible general
environmental damage caused by lead is difficult to give. One area of
concern that has recently become apparent involves the possible role
played by leaded gasoline emissions in the contamination of shellfish.
At the 1968 Shellfish Sanitation Workshop conducted by the U.S. Public
Health Service, guidelines for trace metals were proposed. Maximum
acceptable levels for trace metals in shellfish were established at 2
milligrams per kilogram (PPM) wet tissue weight for cadmium, lead, mercury,
and chromium (combined). These proposed levels assumed an average
serving of shellfish meats to be about 200 grams (7 ounces on a wet
weight basis). Lead levels in shellfish from many areas have already
been shown to exceed this proposed maximum acceptable level in soft clams,
hard clams, surf clams, and oysters. These data indicate that over 18%
of oysters collected off the shores of two states exceeded the proposed
maximum acceptable lead level. In the Raritan Bay, lead levels in shell- >
fish were approximately 10 times higher than normal. This report concludes
that contamination of edible shellfish by heavy metals may present a
serious health hazard.
There is mounting evidence that lead from gasoline probably con-
tributes to the lead content of shellfish. A study conducted on contract
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A-30
to EPA indicates that hundreds to thousands of pounds of lead particulate
matter fall out from the air to the ground, and are then regularly washed
2
off the street during heavy rainstorms. These street washings contain-
ing large amounts of lead eventually reach our waterways through the
sewer systems, where they may potentially contaminate shellfish. Lead
also enters these waterways via improper disposal of petroleum products
containing lead additives directly into sanitary sewers.
Thus there appears to be a relatively rapid turnover of lead
contaminated street dirt via periodic rainstorm washing of streets.
Reductions in the use of lead as a gasoline additive can be expected
to decrease the concentrations and total amounts of lead currently
found in urban street dirt. Consequently, decreases in lead water
pollution are also anticipated by this reduction.
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A-31
REFERENCES FOR APPENDIX A - QUESTION 7
"Metals in Shellfish with Particular Reference to Lead",
prepared by the Northeast Water Supply Research Laboratory of the
U. S. Environmental Protection Agency, p. 17.
p
"Water Pollution Effects of Street Surface Contaminants,"
EPA Contract #14-12-921, prepared by URS Research Co., January 1972,
Draft of Final Report.
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APPENDIX B A SURVEY OF AIR AND POPULATION LEAD LEVELS IN SELECTED
AMERICAN COMMUNITIES (SEVEN CITY LEAD STUDY)
In 1961, a special study to evaluate the problem of atmospheric
lead in urban areas was begun. Blood and urine samples from selected
populations in the cities of Cincinnati, Los Angeles and Philadelphia
were analyzed for their lead content and these data were compared to
atmospheric lead levels to which these people were exposed.
This study (often referred to as the "Three City Study") con-
cluded (1) that a definite difference in atmospheric lead levels
existed between urban and rural areas with highest levels being re-
corded in the central city and (2) that increased blood lead levels
were measured among people working or residing in urban areas
compared to people in rural areas.
Seven years after completion of the Three City Study, a follow-up
investigation was begun to determine whether atmospheric lead levels
had changed significantly with time and if blood lead continued to
be elevated in regions of high atmospheric lead levels. This work
was carried out by the Kettering Laboratory of the University of
Cincinnati and was supported by the American Petroleum Institute,
the International Lead Zinc Research Organization and the Environmental
Protection Agency. Sampling sites used in 1961-1962 were reestablished
and additional sampling sites were set up in the original three cities
as well as in five new cities including Los Alamos, Chicago, Houston,
New York and Washington, D. C. A comprehensive preliminary report of
these data (referred to as the "Seven City Study") was presented at
the EPA Los Angeles Public Hearing on May 3, 1972.
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B-2
The following analysis represents initial comments by Agency
staff regarding the results of this study. Much testimony was
presented during the public hearings and subsequent comment periods
that the Seven City Study failed to demonstrate any significant
relationship between air lead exposure and blood lead level. While a
significant correlation between blood lead and air lead was not found
when all geographical areas were compared, within each area blood lead
levels were consistently elevated among urban residents as compared
to those residing in the surburbs.
EPA does not believe that failure to demonstrate a significant
correlation between blood lead and air lead in this study proves that
no relationship exists between blood lead and air lead. A significant
correlation would never be expected to result from this particular
investigation in part because a wide enough air lead exposure range
was not examined. The observed increases in blood leads among urban
residents compared to suburban residents supports the probable con-
tribution of airborne lead in establishing this difference.
When discussing these results one key factor must be kept carefully
in mind. That is, although food and water contribute more to lead
absorption than air at low air lead exposures, if lead intake from
food and water can be kept reasonably constant, then differences in
blood leads can be more easily detected. Variation of dietary lead
intake tends to be greater between geographic areas than within
geographic areas. Hence urban-suburban comparisons are less confounded
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B-3
by differences in dietary lead intake, thus increasing the probability
of detecting differences in blood lead due to variable air lead ex-
posures. This in part accounts for the failure to obtain a significant
correlation between areas while within areas consistent effects of
increased air lead exposures upon blood lead were found.
Since lead intake from food and water among areas in this study,
as measured by fecal lead excretion, varied considerably, correlations
between air lead and blood lead would not be expected to be very signi-
ficant, especially at small air lead gradients. Although differences
in fecal lead excretion were not always in a direction that could
explain specific area inconsistencies, the very existence of this
factor in part explains why a statistically significant correlation
was not observed.
Another important consideration related to data analysis from the
Seven City Study is that many thousands of individual data points were
reduced into approximately one dozen simple average blood lead levels,
which were then correlated with air lead exposures averaged over time.
This averaging procedure resulted in the loss of a considerable amount
of information present in the original data. Consequently, these re-
sults were reduced to a series of averages which did not adequately
describe the real world from which they originated. This is especially
important when one considers that, although average blood leads in a
given group may be well within normal limits, selected individuals
within that group may have blood leads that are elevated above normal.
Any averaging that is done during analysis will tend to obscure the
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B-4
presence of abnormally elevated blood leads in the original data.
Further, had all of the original data points been plotted instead of
just the averages, a statistically significant correlation between air
lead and blood lead could possibly have been obtained. Comparing blood
lead determinations to yearly average air lead exposures derived from
monthly measurements which varied considerably is also not appropriate
from a physiologic standpoint since blood lead is most likely a function
of air lead exposures taken 2-3 months before blood leads are sampled.
Important conclusions regarding the study become more apparent when
additional methods of data analysis are employed. For example, the
hypothesis that urban and suburban exposure categories are alike with
respect to observed blood lead levels can be tested by considering how
many individual blood leads are above a given blood lead value by using
a Chi squared analysis. This frequently used and commonly accepted
statistical technique will readily demonstrate any differences in
blood leads between groups as this relates to residence and consequent
exposure to differing quantities of airborne lead.
Three urban-suburban comparisons can thus be established. In each
instance the number of people with blood leads above 21.8 micrograms per
hundred grams in urban versus suburban areas are compared. There is
nothing magic about the choice of 21.8 as a cutoff in this test. This
cutoff was chosen because it was well toward the middle of each distri-
bution but slightly toward the side of higher blood lead levels.
Consequently, any trend toward elevated blood leads in one group compared
to the other becomes more apparent.
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B-5
Table B-1 - Philadelphia
Urban - Suburban Blood Lead Comparison
Number of People
Blood lead less than
21.8
Blood lead greater than
or equal to 21.8
Urban
76
60
136
Suburban
105
45
150
181
105
286
X =6.12 (Idf)
.01 p .02* (*Statistically significant)
Average Air Lead Average Blood Lead
(ug/m -geometric mean) (ug/IOOg -geometric mean)
Philadelphia Urban
Philadelphia Suburban
1.67
1.15
20.5
18.0
Philadelphia Urban
Philadelphia Suburban
% Blood leads 29ug/100g &
Above
11.0
4.7
% Blood Leads 40ug/100g &
Above
1.5
0
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B-6
Table B-2 - Chicago
Urban - Suburban Blood Lead Comparison
Number of People
Urban
Suburban
Blood lead
<• 21.8
Blood lead
£21.8
118
29
147
200
8
208
318
37
355
X =23.3 (Idf)
p <: 0.01*
Average Air Lead
(ug/m -geometric mean)
Chicago Urban 1.76
Chicago Suburban
1.18
(*Statistically significant)
Average Blood Lead
(ug/IOOg -geometric mean)
17.6
13.9
Chicago Urban
Chicago Suburban
%B1ood Leads 29ug/100g & Above %Blood Leaas 40ug/100g & Above
3.4 0.7
0.5 0
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B-7
Table B-3 - New York
Urban - Suburban Blood Lead Comparison
Number of People
Blood lead
<21.8
Blood lead
^21.8
Urban
119
21
140
Suburban
180
18
198
X2=2.81
O.OScp* 0.10
299
39
338
Average Air Lead
(uq/m -geometric mean)
New York Urban
New York Suburban
2.08
1.13
Average Blood Lead
(ug/IOOq -geometric mean)
16.6
15.3
New York Urban
New York Suburban
% Blood Leads 29ug/100g
and Above
1.4
0.5
% Blood Leads 40ug/100g
and Above
0
0
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B-8
In two of the three comparisons (Philadelphia and Chicago)
statistically significant differences in blood lead patterns between
groups are present in urban as compared to suburban residents. In
the third comparison, New York, although statistical significance.was
not achieved at the 5% level, the results are very close to being
significant.
In each of these comparisons the urban residents as a-group had
I
greater numbers (and percentages) of people with blood leads greater
i
i
or equal to 21.8ug/100g than those in the suburban groups. Thus a
statistically significant trend toward higher blood lead levels among
urban residents exposed to higher levels of airborne lead is evident.
A second important observation is that only in urban areas are more
individual blood lead levels found to be near or above the level indica-
tive of excessive lead exposure in adults (blood lead of 40ug/100g or above).
Further, the Seven City Study concluded that men have higher blood
lead levels than women at comparable air lead exposures. (Approximately
2ug/100g greater on the average.) Thus, had men been studied instead of
women, a greater percentage would have been found to have abnormally
elevated blood lead levels (40ug/100g and above). If these findings
can be extrapolated to the general urban population, one must conclude
that several million adults are probably excessively exposed to lead as
a result of residence in urban environments where airborne lead exposures
tend to be elevated.
As a result, the Seven City Study suggests the possibility that
despite measurements showing that average blood leads in the United
States are well within normal limits, there apparently are large numbers
of urban adult Americans who are presently excessively exposed to lead.
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B-9
REFERENCES TO APPENDIX B
Survey of Lead in the Atmosphere of Three Urban Communities,
Public Health Service Publication , No. 999-AP-12.
9328
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