ERRATA
Page 5, para. 1, line 5: Change note "35/" to read "34/."
Page 5, para. 1, line 5: Following the sentence eading:
",..per 100 grams of whole blood 34/." insert" "Subtle
signs of clinical lead poisoning have been associated with
blood lead levels of about 50 to 80 micrograms/per 100 grams
of whole blood.(35)"

Page 5, para. 4 line 9: Following the sentence ending
",,. accumulating lead in their bodies." insert "40/"

Page 8, para. E, lines 1 and 7: Change "Kg" to "kg."

Page 17, reference 61: After "Amer. J. Dis. Child." omit:
"122" and insert: "Vol. 122, October, 1971, pp. 337-340."

REFERENCES

In the "Health Hazards of Lead" paper, the references to the

National Academy of Sciences (NAS) report, "Airborne Lead in
Perspective," included page numbers which referred to the pre-
publication copy. Recently the NAS report has been published in
final form. Accordingly, the references to the NAS report have
been revised and listed below to refer to the appropriate page
of the published version of "Airborne Lead in Perspective."

1.

13,
13a
13a
14.
15.
16.
24,
29.

32.

National Research Council-National Academy of Sciences.
"Lead, Airborne Lead in Perspective," A Report Prepared by
the Committee on Biological Effects of Atmospheric Pollutants
of the Division of Medical Sciences, 1971 (NAS Report). All
NAS page references refer to the published copy.

NAS Report, p. 22.

ibid p. 24.

ibid p. 27.

ibid p. 28.

ibid p. 30.

ibid p. 50.

NAS Report, p. 46.

NAS Report, p. 69.

ibid p. 48.

NAS Report, p. 69. (Precise numbers deleted in final report, but
general context of the quote remains the same.)


14

TABLE 7

Relationship. of Adult. Blood Lead Levels and. °
Body Lead Burdens to Airborne Lead Exposure

Air Lead Daily Lead Absorption. Expected
Exposure ug/day Blood Lead?

‘ Relative Excess in
ug/n> Airl Diet? Total u/g100g Blood Lead (%)4
2.0 13.8 30 43.8 21.3 ‘ 0%

2.5 17.3 30 47.3 22.8 7%
3.0 20.7 30 50.7 24.3 : 15%
3.5 24.2 30 54.2 25.8 23%
4.0 27.6 30 57.6 27.3 30%
4.5 31.1 30 61.1 28.8 38%
5.0 34.5 30 64.5 30.3 47%
10.0 69.0 30 99.0 40.0 137%
20.0 138.0 30 168.0 53.8 284%
50.0 345.0 30 375.0 71.6 780%
100.0 690.0 30 720.0 87.2 ~ 7. 1550%

1/ Assumes inhalation of 23 m3/day and 30% lung retention.

2/ Assumes 10% gastrointestinal absorption of the average adult deily total
dietary intake (300 ug) from food and water.

3/ Computed from regression formula: Blood lead = 69.2052 + 54.7605 x log ug Pb
absorbed daily as given in Chapter 3 of Airborne Lead in Perspective by the,
National Research Council, National Academy of Sciences.

4/ Relative excess in blood lead is associated with ambient air exposure
above 2.0 ug Pb/m3.


fe 5

An individual's total daily lead absorption is calculated by adding daily
dietary lead absorption (about 30 micrograms) to the amount absorbed from air.

For convenience, these calculations have been summarized over a wide range
of airborne lead levels (Table 7). Elevated blood leads and thus excess body
burdens are associated with airborne lead levels greater than 2.0 micrograms per
cubic meter. Increased urinary excretion of delta-aminolevulinic acid begins at
blood lead levels of about 40 micrograms per 100 grams of whole blood. (34)
Subtle signs of clinical lead poisoning have been associated with blood lead
levels of about. 50 to 80 micrograms/per 100 grams of whole blood. (35)

At the present time, there are no epidemiologic data which relate the
lead concentration in the blood of infants and children to their estimated
exposure to atmospheric lead.

B. Health Effects

Lead accumlates in humans when the amount they absorb from all sources
exceeds the amount that is excreted. Clinical experiments have demonstrated that
small increments in the amount of lead in the diet will result in prolonged (though
not indefinite) periods of accumulation. (28) Presumably, increments in the amount
of lead absorbed from the lungs will result in similar periods of accumulation of
lead in the body. Certain occupational groups (garage workers, auto mechanics,
and vehicular tunnel policemen) who are incidentally exposed to high atmospheric
lead concentrations have been found to have mean blood levels of lead that are
higher than the mean of the general population. (36,37) Furthermore, several
studies have shown that urban residents have a higher average level of lead in
their blood than their rural counterparts. (36,38) Although this difference might
be due to differences in dietary lead intake between the :groups,(39) it might also
be due to differences in the intake of lead from the air, In either event, it
is clear that most people are accumulating lead in their bodies. The NAS Report
concluded: "The exposure of people in the general population to lead results in
some accumulation in the body up to and perhaps beyond the age of 40, as deter-
mined by analysis of tissues." It goes on to say: "The biologic significance
and reason for the increase are not known." (40)

Overt symptons of clinical lead poisoning in adult males have not been
reported at levels of lead in the whole blood lower than 80 micrograms/100 grams.
However, inhibition of the activity of certain enzymes involved in the synthesis
of heme can be shown to occur when the levels of lead in the whole blood are less
than 80. micrograms/100 grams. For example, the inhibition of aminolevulinic acid
dehydrase (ALAD), (41) the enzyme which catalyzes the conversion of delta-amino-
levulinic acid (ALA) to porphobilinogen (PBG), occurs well below 80 micrograms/
100 grams of blood. There is an inverse linear relationship between the logarithm
of the activity of ALAD in vitro and the concentration of lead in the blood when
the concentration varies from 5 to 95 microgram/100 grams. (42,43,44) Although
ALAD is essential for hemoglobin synthesis at lead concentrations below 40 micro- |
grams/100 grams, there are currently no detectable biological effects of this
enzyme inhibition.(45) This does not prove that no biological effects occur.

However, when the levels of lead in the blood exceed 40 micrograms/100
grams, the amount of ALA excreted in the urine increases exponentially. (46,47)
The NAS Report hypothesized that: "The exponential increase in ALA excretion
associated with blood lead content above approximately 40 micrograms/100 grams


34,
35.
39.
40.
41.
45.
48,
49.
55.

60.
62.
63.
64,
65.
66.
67.

NAS Report p. 107.
ibid p. 74.

NAS Report p. 63.
ibid p. 67.

ibid p. 106

NAS Report, p. 208
NAS Report, p. 110.
ibid p. 208.

NAS Report, p. 139.
ibid p. 140.

NAS Report, p. 74
NAS Report p. 110.
ibid p. 132.

ibid p. 211,

ibid p. 139.

ibid p. 211.

ibid p. 208.


Corrections and Additions
To
Health Hazards of Lead :

(Revised April 11, 1972)

Prepared by

U. S. Environmental Protection Agency
Office of Air Programs, Rockville, Md.,
and
National Environmental Research Center
Division of Health Effects Research
Research Triangle Park, North Carolina

April 27, 1972


TABLE 1

Lead consumption in the U. S., 19684

Product category Tons consumed
Metal products? 915,500
Pigments 109,734
Gasoline additives 261,897
Other —~ 41,659
TOTAL 1,328,790

a/ Adapted from Minerals Yearbook, 1969, p. 47
b/ Includes 513,703 tons consumed for storage batteries

TABLE 2

Lead emission in the U. S., 1968?

Emission source Lead emitted, tons/year
Gasoline combustion 181,000
Coal combustion 920
Fuel oil combustion 24
Lead alkyl manufacturing 810
Primary lead smelting 174
Secondary lead smelting 811
Brass manufacturing . 521
Lead oxide manufacturing : 20
Gasoline transfer 36
TOTAL 184,316

a/ Data from National Inventory of Air Pollutant Emissions
and Controls, on file at the Environmental Protection Agency,
Stationary Source Pollution Control Program, Durham, N. C.


lead poisoning in children is not clearly defined, the NAS report states:
"Airborne lead wastes from such sources as: automotive emissions and the weather-
ing and demolition of old buildings can be expected to have a significant addi-
tive effect on the total intake."(56) It should be remembered that combustion
of gasoline containing lead additives is responsible for 98 percent (57)of the
emissions of lead to the atomosphere.

The clinical manifestations of lead poisoning are variable and reflect
involvement of several different organ systems. They include anemia, acute
abdominal colic, acute encephalopathy, chronic encephalopathy, peripheral
neuropathy, and chronic nephropathy. The syndromes of acute lead poisoning
usually resolve following cessation of the exposure to lead and institution of
therapy. However, acute encephalopathy in young children is followed by perma-
nent neurological sequelae in at least 25. percent of the cases.(58,59)

In virtually all of the cases of human lead poisoning recorded to date,
it has not been possible to quantitate the amount of lead absorbed prior to
the onset of symptoms. Balance studies in human volunteers have shown that
the blood lead level is a fairly sensitive index to recent, absorption of lead.
Overt symptons of clinical lead poisoning have not been reported at blood lead
levels below 80 micrograms/100.grams (in occupationally exposed adult men who
are not anemic and are otherwise healthy). However, symptoms and signs
compatible with mild lead poisoning have been. associated with whole blood
concentrations of 50-80 micrograms/100 grams.(60) In 41 cases of acute lead
poisoning in children, the average blood lead value was 176 micrograms/100 grams,
with the lowest value being 63 micrograms/100 grams. In-99 cases of encephalo-
pathy, the average blood lead level was 330 micrograms/100 grams. (61)

7. Summary and conclusions

A. Lead has not been shown to have any biologically useful function;
all available data indicate that the metabolic effects of low
concentrations of lead are of the inhibitory or adverse type. Accord-
ingly, any increase in body burden of lead is: accompanied by an
increased risk of human health impairment.

B. Though the amounts of lead ingested in the diet generally are
greater than the amounts inhaled, the body absorbs a greater
percentage of inhaled lead (30 percent or more) than of ingested
lead (about 10 percent).

C. Human blood lead levels are the most frequently used index of human
exposure to environmental lead; it should be noted, however, that
other tissues, e.g., hair, may provide a more accurate index of
total body burden, particularly where exposure levels are relatively
low.

D. Human blood lead levels begin to rise appreciable with exposure
to airborne lead concentrations in excess of 2 micrograms per
cubic meter. Table 1 reflects the best available data on the
relationship of lead intake to absorption and blood lead levels.


of whole blood signifies inhibition of ALAD that is physiologically significant
in vivo." (48) With respect to hematopoiesis, this inhibition of the conversion
of ALA to PBG may be compensated completely when the concentration of lead in
whole blood ranges between 40-80 micrograms/100 grams. However, when the level
of lead in the blood exceeds about 80 micrograms/100 grams, the compensatory
mechanism becomes inadequate and anemia ensues. The NAS Report states the
following concerning the inhibition of ALAD (and the resulting excretion of

ALA in the urine) at blood lead concentrations of 40-80 micrograms/100 grams:"
...this action must be viewed as undesirable, in that it does represent an
inference with the availability of an essential metabolite required for normal
body function, which in some circumstances might prove deleterious." (49) The
risks from ALAD enzyme inhibition are increased among inner city children. These
children are deficient in iron intake, which further decreases red blood cell
synthesis, and are exposed to higher levels of carbon monoxide, which reducés the
oxygen carrying capacity of their blood.

Three groups include most of the cases of clinically recognizable lead
poisoning in the United States. These groups are young children living in urban
areas; people who consume illicitly distilled, lead-contaminated alcohol; and
workers in the lead trades. Additional sporadic cases of lead poisoning have
been caused by the burning of battery casings in the home and the use of earthen-
ware which has been improperly finished with a lead-containing glaze.

Young children living in deteriorating, dilapidated, urban housing are at
risk to be poisoned by lead because of their indiscriminate eating habits and
the availability of lead in their environment. The usual source of lead in cases
of poisoning among such children is lead-pigment paint flaking from the interior
surfaces of the dwellings in which the children live. (50) These paint flakes
contain as much as 40 percent lead by weight.

Mass-screening programs conducted in New York and Chicago(51,52)have shown
that between 1 and 2 percent of the children examined have blood levels of lead
that are compatible with lead poisoning. In addition, 25 percent of the children_
have levels of lead in their blood that exceed the upper limit of normal (40 micro-
gram/100 grams). (52) Although the direct ingestion lead-pigment paints is the
principal environmental source in cases of severe lead poisoning in young children,
it may not explain the rather large percentage of children with levels of lead
in the blood exceeding 40 microgram/100 grams. Other potential sources of lead
intake in the urban environment are lead in the atmosphere and lead that "falls
and rains out" of the air and is contained in the dust on the ground. Dustfall
samples fall from 77 midwestern cities contianed the following average amounts
of lead: In residential areas - 1,636 micrograms/grams of dust; in commercial
areas - 2,413 micrograms/grams of dust; and in industrial areas - 1,512 micro-,
grams/grams of dust.(53) It has been calculated that daily ingestion by a
one-year-old child of as little as 1/24 of a teaspoon of dust from within 100
feet of a busy roadway would, within eight months, result in lead poisoning. (54)
The NAS report stated: "The swallowing of lead-contaminated dust may well
account, in large part, for the higher mean blood lead content in urban children
and the rather large fraction whose blood lead content falls in the range of 40-
60 micrograms/100 grams of whole blood, thereby bringing them into the range in
which increased urinary excretion of ALA may be observed."(55) Although the
extent to which airborne lead in urban air contributes to lead absorption and


The original Table 7 on page 14 should be replaced by the following revised
and corrected Table 7. The figures presented in the original Table 7 for expected
blood lead concentrations and relative excess in blood lead percentages were
miscalculated and have been corrected. Footnote 4 has also been revised.

TABLE 7

Relationship of Adult Blood Lead Levels
to Airborne Lead Exposure

Air Lead Daily Lead Absorption Expected
Exposure ug/day Blood Lead:

Relative Excess in
ug/m> airt Diet” Total ug/100g Blood Lead (ay
2.0 13.8 30 43.8 20.7 0%

2.5 17.3 30 47.3 22.5 %

3.0 20.7 30 50.7 24.2 17%

3.5 24.2 30 54.2 25.8 25%

4.0 27.6 30 57.6 27.2 31%

4.5 31.1 30 61.1 28.6 38%

5.0 34.5 30 64.5 29.9 44%,
10.0 69.0 30 99.0 40.1 94%
20.0 138.0 30 168.0 52.7 155%
50.0 345.0 30 375.0 71.7 246%
100.0 690.0 30 720.0 87.3 322%

1/ Assumes inhalation of 23 m3/day and 30% lung retention.

2/ Assumes 10% gastrointestinal absorption of the average adult daily total
dietary intake (300 ug) from food and water.

3/ Computed from regression formula: Blood lead = -69.2052 + 54.7605 x log
ug Pb absorbed daily as given in Chapter 3 of Airborne Lead in Perspective
by the National Research Council, National Academy of Sciences.

4/ According to the National Academy of Sciences, ". . . it is not possible,
on the basis of available epidemiological evidence, to attribute any
increase in blood lead concentration to exposure to ambient air below a
mean lead concentration of about 2 or 3 ug/m . . ." 64/ It follows that
a relative excess in blood lead may be associated with ambient air exposure
above 2.0 ug Pb/m’.


Based on the available evidence,:the. Administrator has concluded
that airborne lead levels exceeding 2 micrograms per cubic meter, averaged
over a period of three months or longer, are associated with a sufficient
risk of adverse physiologic effects to constitute endangerment of public
health. Since airborne lead levels in many major urban areas currently
range from 2 to somewhat over 5 micrograms, and since motor vehicles are
the predominant source of airborne lead in such areas, attainment of a
2.0 microgram level will require a 60 to 65 percent reduction in lead
emissions from motor vehicles.


HEALTH HAZARDS OF LEAD
1. Int roduct ion

This paper contains a summary and analysis of all relevant medical and
scientific evidence available to the Environmental Protection Agency (EPA) as
of January 1, 1972, on the health hazards of airborne lead. As background,
the paper also includes information on sources of airborne lead and lead levels
in the environment. The information presented in this paper is drawn from
several sources including a comprehensive report(1)prepared for EPA by the
National Research Council-National Academy of Sciences; throughout this paper,
the report will be referred to as the NAS Report. It should be noted that the
conclusions presented in the final section of this paper are EPA's conclusions.

2. Sources

Naturally occurring lead in the atmosphere results from airborne dust,
which contains on the average 10-15 ug of lead per gram of dust,(2)and from
gases diffusing from the earth's crust.(3) These contribute about 0.0005 ug/m3
of lead to the atmosphere. (4)

The 1968 consumption of newly extracted and recycled lead in the United
States was about 1.3 million tons.(5) The largest consumer was the electric-
storage-battery industry (39%), followed by the petroleum industry, which used
about 20% of the total for gasoline additives.(5) The amount of lead consumed
in various products in 1968 is shown in Table 1. Table 2 shows estimated
lead emissions in 1968 from most of the significant known sources. Annual
consumption of lead for use in gasoline additives has increased by 65% over
the past 10 years and has more than quadrupled since 1943. (6) As indicated
by the data in Tables 1 and 2, only about 20% of the lead consumed in 1968
went into petroleum products, but almost 99% of the estimated lead emissions
to the atmosphere were from gasoline combustion, gasoline transfer, and gaso-
line antiknock additive manufacturing, with over 98% of the emissions coming
from gasoline combustion alone.

3. Ambient air levels

The concentration of lead in ambient air is closely correlated with the
density of automotive traffic. Thus, concentrations are highest in large cities
at sites of heaviest traffic and generally are progressively lower in suburbs,
smaller towns, and rural areas. An extensive study of ambient air levels in
Los Angeles, Cincinnati, and Philadelphia has been carried out.(7) Sampling
sites were located in representative rural, residential, commercial, and
industrial areas, and sampling was performed continuously from June 1961
through May 1962. The results are summarized in Tables 3 and 4.

In the three-city survey,(7) a special, less extensive study, designed
to measure atmospheric lead concentrations found in heavy traffic, was conducted.
This study showed a clear diurnal pattern related to commuter rush hours. The
pertinent data are presented in Table 5.

The National Air Surveillance Networks (NASN) of the Environmental
Protection Agency continually sample the atmosphere for lead and other


TABLE 5

Atmospheric Concentrations of Lead in Traffic
in Cincinnati arid Los Angeles@

Concentration, ug/m

12

Morming Rush Midday Aftemoon_ Rush
, No. of No. of No. of
City Mean Range Samples Mean Range Samples «Mean Range Samples
Cincinnati -
Mobile Routes 14.2 7.2- 20 9.1 7.0- 8 15.2 9.3- 8
19.5 12.3 21.1
Los Angeles
Freeway 38.0 26.9- 7 24.1 16.6 7 18.4 8.7 7
54.3 31.1 25.4
Downtown 23.6 19.1- 6 10.5 8.4- 4 15.3 12.4- 4
29.9 12.2 18.6

a/ Taken from "Survey of Lead in the Atmosphere of Three Urban Communities",
ref. 1, pp. 55-56,


TABLE 3

Annual Mean Concentrations of Atmospheric Lead
June 1961 through May 19628

Lead concentration, ug/m>

Site Cincinnati Los Angeles . Philadelphia
Commercial 1.7 2.9 2.2
Industrial 1:8 2.3 2.2
Residential 1.1 2.0 1.1
Rural 0.9 2.8 0.9
All Stations 1.4 2.5 1.6

a/ Adapted from "Survey of Lead in the Atmosphere of Three Urban
Communities," reference 7, p. 32.

TABLE 4

Seasonal Mean Concentrations of Atmospheric Lead
June 1961 through May 19624

Lead concentration, ug/m>

Season Cincinnati Los Angeles Philadelphia
Summer 1.3 1.9 1.4
Fall 1.7 2.8 1.9
Winter 1.3 3.1 1.9
Spring 1.3 2.1 1.4

a/ Taken from "Survey of Lead in the Atmosphere of Three tirban
Communities," reference 1, p. 32.

il


Elevated lead intake for periods as short as, and possibly shorter
than, three months is sufficient to produce an increase in blood
lead levels.

Average blood lead levels tend to be higher among urban residents
than among rural residents; they also tend to be higher among
certain occupational groups, i.e., garage workers, auto mechanics,
vehicular tunnel policemen, than among the general population.

Body burdens of lead, as measured by bone lead concentrations,
are known to increase with age at least until age 40 and probably
thereafter.

The activity of certain enzymes involved in heme synthesis (one step
in red blood cell formation) is inhibited at blood lead levels signi-
ficantly below those associated with clinical lead poisoning; speci-
fically, when blood lead levels exceed 40 micrograms per 100 grams,
the amount of ALA excreted in the urine begins to increase exponentially.
According to the NAS report: "The exponential increase in ALA excre-
tion associated with blood lead content above approximately 40 micro-=
grams/100 grams of whole blood signifies inhibition of ALAD that is
physiologically significant in vivo".(62) The NAS report also
contained the observation that "...this action must be viewed as
undesirable, in that it does represent an interference with the
availability of an essential metabolite required for normal body
function, which in some circumstances might prove deleterious."

Exposure to airborne lead often tends to be greatest in areas whose
inhabitants, particularly children, are especially likely to be
exposed to other environmental sources of lead.

Though ingestion of leaded paint clearly is the principal cause

of lead poisoning among children, it does not necessarily account

for the rather large percentage (25 percent) of children who, in
mass screening programs in inner city areas, did not appear to

have clinical lead poisoning but had blood lead levels exceeding

40 micrograms per 100 grams. Among such children, the high concen-
trations of lead found in urban street dust are another potential
source of lead intake. According to the NAS report: "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 content falls in the range of 40-60 micro-
grams per 100 grams of whole blood, thereby bringing them into the
range in which increased urinary excretion of ALA may be observed."

The elevated concentrations of lead in dust, soil, and vegetation
near streets and highways clearly can be attributed to lead emissions
from motor vehicles.

Precipitation samples from 32 locations in the U.S. showed a positive
correlation between gasoline consumption and lead content of precipi~
tation in the areas where the sampling sites were located.


Only a fraction of the lead balance ingested in the diet is absorbed
from the gastrointestinal tract. Lead balance studies in adults have shown
that the average absorption of lead from the gastrointestinal tract over
long periods of time is 5-10 percent of the ingested dose when the lead
intake is not excessive. (28) Therefore, it can be calculated that about 15
to 30 micrograms of lead are absorbed from the diet each day by an adult.
The exact proportion of dietary lead intake that is absorbed by infants
and children has not been determined.

The contribution of lead in the air to the total amount absorbed each
day has not been precisely defined. For adults, estimates of the contribution
have been made by assuming that: 1. Similar percentages of lead particulate
matter will be deposited in the respiratory tree, regardless of the concentra-
tion of lead in the inhaled air (Experiments with air containing 150 ug/m3. of
lead particulate matter with a mass median diameter of 0.25 um showed that
36 percent of the lead was deposited in the airways.(28) It was then assumed that
a similar percentage of lead would be deposited when air containing concen-
trations of lead in the range of 1-10 ug/m3 was inhaled), and 2. all of the
lead deposited in the respiratory tract is absorbed into the body. From these
assumptions, it can be predicted that the total daily absorption of lead from
the air by a "standard man" engaged in light activity would be from 0.8 ug to
63 ug, depending on where he lives and works. (32) The percentage ‘of inhaled
lead that is deposited in the respiratory tract of infants and children has
not been determined experimentally; however, if it is assumed that the
deposition is similar to adults (i.e. about 36%), and that all the deposited
lead is absorbed into the body, one can calculate the amount of lead is
absorbed from the air.

During periods of normal intake of lead, about 90 percent of the
lead appears in the feces. (28) A small amount of this lead may initially be
absorbed and then excreted back into the gastrointestinal tract. Most of
the remaining dietary lead that is not retained in the body or found in the
feces can be found in the urine.

If certain simplifying assumptions are made, one can construct a dose-
response curve relating the concentration of lead in the blood to the daily
absorption of lead from all sources. The epidemiologic data assembled by
Goldsmith and Hexter (33) are used for lead concentrations in the blood of
various groups of men whose estimated exposure to atmospheric lead differed.
The contribution of lead in the air to the daily absorption is estimated by
using the assumptions mentioned above (i.e., that similar percentages of inhaled
lead particulate matter are deposited in the respiratory tract, regardless of
the concentration of lead in the inhaled air, and that all the lead that is
deposited in the airways is absorbed). Respiratory deposition of inhaled lead
ranges from 25 to 50%. The amount of lead that will be absorbed from inhaled

. air is equal to the airborne lead concentration X the volume of air inhaled per
day (about 23 cubic meters) X the percent of lead deposited in the respiratory
tract. For example, if a person inhales air containing 2 micrograms of lead
per cubic meter, and a conservative 30% respiratory deposition is assumed, then
the lead absorption from the air can be calculated as follows:

2 ug/m3 X 23m3 X 30%= 13.8 micrograms


ll.

12.

13,
13a
13b
14.
15.
16.
17.

18,

19.

15

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National Research Council-National Academy of Sciences, Airborne Lead in
Perspective, A Report Prepared by the Committee on Biological Effects of
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Isotopes in Pelogic Sediments. Geochim. Cosmochim. Acta. 26: 263-308,
1962.

Blanchard, R.L. Relationship Between Polonium - 210 and lead - 210 in Man
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the International Symposium on Radioecological Concentration Processes.

New York. Pergamon Press. 1966 p. 281-294.

Patterson, D.C. Contaminated and Natural Lead Environments of Man. Arch.
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Minerals Yearbook, 1968, Bureau of Mines, Department of the Interior,
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Minerals Yearbooks, 1940-1969. Bureau of Mines, Department of the Interior,
Washington, D.C.

Survey of Lead in the Atmosphere of Three Urban Communities. Public Health
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Air Pollution Measurements of the National Air Sampling Networks; Analyses
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Air Quality Data from the National Air Sampling Networks and Contributing
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Air Quality Data from the National Air Sampling Networks and Contributing
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NAS Report, p. 21.

ibid p. 49.
ibid p. 26.
ibid p. 27.
ibid p. 29,
ibid p. 71

Daines, R.H., H. Motto and D.M. Chilko. Atmospheric Lead: Its Relationship
to Traffic Volume and Proximity to Highways. Environ. Sci. Tech. 4:
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Schroeder, H.A., J.J. Balassa, F.A. Gibson and S.N. Valanju. Abnormal
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Data from the Seven Cities Study. Jointly sponsored by Amer. Petrol. Inst.,
International Lead Zinc Research Organization, and the EPA and carried out
by staff of the Kettering Laboratory, Cincinnati, Ohio.


45.
46.

47.

48,
49,
50.

54,

55.
56.
57.
58.
59.

60.
61.

62.

17

NAS Report, p. 323.

Nakao, K., 0. Wada, and Y. Yano. Delta-Aminolevulinic Acid Dehydrase
Activity in Erythrocytes for the Evaluation of Lead Poisoning. Clin.

Chim. Acta. 19: 319-325, 1968.

Selander, S. and K. Cramer. Interrelationships Between Lead in Blood, Lead
in Urine, and ALA in Urine During Lead Work. Brit. J. Ind, Med. 27:

28-39, 1970.

NAS Report, p. 147.

NAS Report, p. 323.

Griggs, R.C., I. Sunshine, V.A. Newill, B.W. Newton, S. Buchanan and C.A.
Rasch, Environmental Factors in Childhood Lead Poisoning. JAMA 187:
703-707, 1964.

Blanksma, L.A., H.K. Sachs, E.F. Murray, and M.J. O'Connell. Incidence of
High Blood Lead Levels in Chicago Children. Pediatrics 44: 661-667, 1969.
Specter, M.J. and V.F. Guinee. Epidemiology of Lead Poisoning in New York
City - 1970. Presented at the American Public Health Association's 98th
Annual Meeting, Houston, Texas, Oct. 26, 1970. 23 p.

Hunt, W.F., Jro, C. Pinkerton, 0. McNulty and J.P. Creason. A Study in
Trace Element Pollution of Air in Seventy-Seven Midwestern Cities. In:
Trace Substances in Environmental Health, IV., Hemphill, D.D. (ed.).
Columbia. Univ. of Missouri. Press, 1971. p. 56-68.

Shy, C.M., D.I. Hammer, H.E. Goldberg, V.A. Newill and W.C. Nelson. Health

Hazards of Environmental Lead. In-House Technical Report, Community Research

Branch, Bureau of Air Pollution Sciences, Environmental Protection Agency.
NAS Report, p. 179.

NAS Report, p. 180.

National Inventory of Air Pollutant Emissions and Controls: Lead. On
file at the Environmental Protection Agency, Stationary Source Pollution
Control Program. Durham, N.C.

Byers, R.K. Lead Poisoning. Review of the Literature and Report on

45 Cases. Pediatrics 23: 585-603, 1959.

Chisolm, J.J., Jr. and H.E. Harrison. The Exposure of Children to Lead.
Pediatrics 18: 943-957, 1956.

NAS Report, p. 108.

King, B.G. Maximum Daily Intake of Lead Without Excessive Body Lead
Burden in Children, Amer. J. Dis. Child. 122

NAS Report, p. 147. .


The concentration of lead in atmospheric dustfall and in surface soil
of large cities, presumably brought about by emissions from automobiles,
can be very high. In Cincinnati at a distance of 25 feet from the roadway,
the average lead concentration was 3397 ug/g, and at least 100 feet, the
average was 2825 ug/g.(20) The concentration of lead in surface soils in
a number of West Coast city parks ranged from 194 ug/g to 3,357 ug/g.(15)

The diet is another source of lead. Schroeder and co-workers(18) have
made extensive determinations of lead in food. On a fresh-weight basis, they
found about 1.2 ug/g (range, 0-1.5 ug/g) in condiments, 0.5 ug/g (range, 0.2-
2.5 ug/g) in fish and seafood, 0.2 ug/g (range, 0-0.37 ug/g) in meat and eggs,
0.4 ug/g (range 0-1.39 ug/g) in grains, 0.2 ug/g (range, 0-1.3 ug/g) in
vegetables, and no lead detectable by their analysis in fresh whole milk.
Continuous monitoring of the water supplies of the United States since 1962
has demonstrated that their lead content has, in general, not exceeded the
U.S. Public Health Service's prescribed standard of 50 ug/liter.(21) Using
these data, and other information, a number of workers (16) have estimated
that the dietary lead intake of an adult averages about 300 ug/day.

5. Environmental cycling

Lead is removed from the air by gravitational settling of larger particles,
by clumping of smaller particles (aggregation) with subsequent settling, and ——
by association with rain or other forms of precipitation as condensation
nuclei or by wash out. Lead emitted in automobile exhaust causes a pronounced
lead concentration profile in surfaces near heavily traveled highways. (22)

The lead content of precipitation is strongly associated with the use of
lead additives in gasoline. Atmospheric precipitation samples from 32 U.S.
stations showed a positive correlation between the number of gallons of gaso-
line used and the concentration of lead in the precipitation of each area. (23)

Plants do not take up substantial amounts of lead from the soil or
atmosphere or from deposits on foliage. The concentration in soil has very
little effect on the lead content of the tissues, (24) except under certain
soil conditions including high acidity and high organic matter content.

6. oman Health Implications
A. Metabolism

The major source of lead intake for non-occupationally exposed adults is
the diet. The average lead content of food is 0.2 parts per million, (25,26)and
the daily average adult oral intake of lead from food is about 300 micrograms,
with a range of 100 to 500 micrograms. (27,28) Limited data indicate that this
intake has not changed significantly in the past thirty years. (29) The daily
intake of lead from water has been estimated to be about 20 micrograms. (30)

The dietary intake of lead by children between the ages of one and three
has been estimated to be 1300 micrograms/day. (31) This estimate was based on
measurement of the amount of lead excreted in the feces by children who had
known no unusual exposure to lead.


pollutants in many parts of the United States. NASN data also tend to show
that lead levels are higher in cities than in rural and remote non-urban areas.
In most cities of the NASN, the annual average concentration of lead in the
atmosphere in 1957-66 ranged from 1 to 3 ug/m3, non-urban stations averaged
0.1 - 0.5 ug/m3 and the concentration at remote stations often less than 0.05
ug/m3. (8-12)

There is evidence (28) that short-term averages are more meaningful than
annual averages as indices of significant human exposure to lead. NASN data
for 1967 and 1969, as shown in Table 6, indicate that there were a minimum of
27 areas where one or more quarterly composite lead concentrations exceeded
2.0 micrograms per cubic meter. In the areas listed in Table 6, NASN sites
were at locations where motor vehicle emissions clearly were primarily or largely
responsible for the measured airborne lead levels. The concentration of lead in
ambient ait is heaviest near highways and is roughly proportional to the volume
of traffic on these highways. A study by Daines, Motto and Chilko, (17)involving
ambient air sampling along a 28-mile section of U.S. 1 in New Jersey in 1967-
69, showed that ambient air levels approaching 10 ug/m3 occur within 10 feet
of a highway with a volume of 58,000 vehicles per day but that the concentra~
tion falls off rapidly as traffic volume decreases or distance from roadway
increases. :

The NAS report states that available data suggest that the concentration
of lead in air, even over most of the larger cities, is increasing only slowly.(13)
The increase in the consumption of lead antiknock additives for gasoline from
169,000 tons in 1962 to 262,000 tons in 1968(13a) indicates that more lead is
being emitted into the atmosphere and suggests that the quantity of lead in ‘the
air can be expected to be higher. Recent data show that in at least three U.S.
cities, lead’ levels increased significantly from 1962 to 1969. Atmospheric
lead- concentrations were measured in 1969 at 19 of the sites where such
measurements were made in 1962 in the original survey of lead in the air
in Cincinnati, Los Angeles, and Philadelphia.(19) An increase of varying magni-
tude over the 7-year period was noted at 17 of the sampling sites. The increases
were statistically significant at 14 sites, and these increases ranged from 33
to 64 percent in Los Angeles, from 25 to 36 percent in Philadelphia and from
26 to 33 percent in Cincinnati.

4. Levels in water and food

It seems likely that, today, the global mean content of naturally occur-

ring lead in lakes and rivers lies between 1 and 10 ug/liter. (13b) The ‘average
lead content of 22 water samples of major rivers of North America was 6.6ug/
liter; and 440 lake and river water samples in Maine was 2.3 ug/liter (range, |
0.03-115 ug/liter).(13b) The natural concentration of lead in soils usually
ranges from 2 to 200 ppm, exclusive of areas near deposits of lead ore.(14)
In addition to fallout from mining, industrial operations, and motor vehicles,
which cause’ localized increases in soil concentrations of lead, soils receive
an average of 1 ug/cm2/year from precipitation and 0.2 ug/cm2/year from dust-
fall. (14)


TABLE 6

Maximum Quarterly Composite Lead Levels Exceeding
2.0 Micrograms Per Cubic Meter@

LOCATION MAXIMUM QUARTERLY COMPOSITE

Oklahoma City, Oklahoma
Baltimore, Maryland
Miami, Florida

Kansas City, Kansas

Fort Worth, Texas
Cleveland, Ohio
Springfield, Massachusetts
Shreveport, Louisiana
Las Vegas, Nevada
Richmond, Virginia

New York, New York
Houston-Galveston, Texas
Seattle, Washington

N. W. Nevada

Detroit, Michigan
Denver, Colorado

Salt Lake City, Utah
Chicago, Illinois

El Paso, Texas
Philadelphia, Pennsylvania
Phoenix, Arizona

San Francisco, California
Puerto Rico

San Diego, California
Fairbanks, Alaska

Dallas, Texas

Los Angeles, California

UNF EEWWWKWWLWKWWNNNNNNNNNNNNN
NN ONNODODADDENDOMMDDAP EHP wWWNP RR

a/ Source: NASN data on file at the Division of Atmospheric
Surveillance, National Environmental Research Center,
Environmental Protection Agency, Research Triangle Park,
North Carolina,


20.

21.
22.
23.

24,
25.

26.
27.
28.
29.
30.
3h.

32,
33.

35.

36...

37.

38.

39.
40,
Al,
42,

43.

16

Shy, C.M., D.I. Hammer, H.E. Goldberg, V.A. Newill, and W.C. Nelson. Health
Hazards of Environmental Lead. In-House Technical Report, Community Research |
Branch, Bureau of Air Pollution Sciences, Environmental Protection Agency,
1971 (to be published).

Public Health Service Drinking Water Standards (Revised 1962). Washington,
D.C. PHS Publ. No. 956. 1969, p. 43-46

Langerwerff, J.V., and A.W. Specht. Contamination of Roadside Soil and
Vegetation with Cadmium, Nickel, Lead, and Zinc. Environ. Sci. Tech. 4:
583-586, 1970.

Lozrus, A.L., E. Lorange and J.P. Lodge, Jr. Lead and Other Metal Ions in
United States Precipitation. Environ. Sci. Tech. 4: 55-58, 1970.

NAS Report, p. 65.
Monier-Williams, G.W. ‘Trace Elements in Food, New York: John Wiley and
Sons, Inc., 1950. 511 pp.

Warren, H.V. and R.E. Delavault. Lead in Some Food Crops and Trees.

J. Sci. Food Agric. 13: 96-98. 1962.

Schroeder, H.A. and I.H. Lipton. The Human Body Burden of Lead. Arch.
Environ. Health 17: 965-978. 1968.

Kehoe, R.A. The Metabolism of Lead in Man in Health and Disease. The
Harben Lectures, 1960. J. Roy. Instit. Public Health Hyg., 24: 1-81,
101-120, 129-143, 177-203, 1961.

NAS Report, p. 94.

ibid p. 69

Barltrop, D. and N.J.P. Killala. Fecal Excretion of Lead by Children,
Lancet 2: 1017-1019, 1967. :

NAS Report, p. 95.

Goldsmith, J.R. and A.C. Hexter. Respiratory Exposure to Lead: Epidemi-
ological and Experimental Dose-Response Relationships. Science 158:
132-134, 1967.

NAS Report, p. 146

NAS Report, p. 108.

Survey of Lead in the Atmosphere of Three Urban Communities. National Air
Pollution Control Administration, Raleigh, N.C. Publ. No. 999-AP-12.
April 1970. 94 p. :

Report of the Swill Leaded Gasoline Commission to the Federal Council on
its Activities During the Period 1947-1960. Translated by the Kettering
Laboratory, Univ. of Cincinnati. Cincinnati, Ohio. Undated.

Goldwater, L.J. and A.W. Hoover. An International Study of "Normal" Levels
of Lead in Blood and Urine. Arch. Environ. Health 15: 60-63, July 1967,
NAS Report, P. 90.

NAS Report, p. 95.

NAS Report, p. 144.

Hernberg, S., J. Nikkanen, G. Mellin and H. Lilius. Delta-Aminolewulinic
Acid Dehydrase as a Measure of Lead Exposure. Arch, Environ. Health 21:
140-145, 1970.

Lichtman, H.C. and F. Feldman. In Vitro Pyrrole and Prophyrin Synthesis in
Lead Poisoning and Iron Deficiency. J. Clin. Invest. 42: 830-839, 1963.
Millar, J.A., R.L.C. Cumming, V. Battistini, F. Carswell, and A. Goldberg.
Lead and Delta-Aminolevulinic Acid Dehydrase Levels in Mentally Retarded
Children and in Lead Poisoned Suckling Rats. Lancet 2: 695, 1970.