EPA1S POSITION ON THE HEALTH
s
IMPLICATIONS OF AIRBORNE LEAD
PREPARED EY
U.S. ENVIRONMENTAL PROTECTION AGENCY
U01 M STREET, S.W.
WASHINGTON, D. C. 20460
NOVEMBER 28, 1973
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ENVIRONMENTAL rr.CTHCTIC:: AGENCY
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TABLE OF CONTENTS
I. Introduction
II. occurrence and Sources of Lead in the Environment
III. Health Aspects of Lead Exposure
IV. Can an Acceptable Lead Body Burden be Defined?
V. Relationship of Environmental Lead Exposure to Human
Lead Intake
VI. Lead Exposure from Dustfall
VII. Extent of Lead Exposure Among the General Population
VIII. Summary and Conclusions
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Introduction
On February 23, 1972, EPA published a notice in the Federal
Register (1), setting forth proposed regulations promulgating
Federal standards for the use of lead and phosphorus additives in
gasoline. Pursuant to the notice, several public hearings were
held. In addition, numerous written comments were received by
the Agency during an extended public comment period. After
consideration of the hearing testimonies and written comments,
and after further consideration of the available information on
health effects of airborne lead, including the adverse effects of-
leaded gasoline on emission control devices, the regulations were
divided into two separate pieces of regulatory action: final
regulations providing for the general availability of lead-free
gasoline were promulgated on January 10, 1973 (2) and regulations
based upon the health effects of airborne lead, providing for the
reduction of lead in leaded gasoline were reproposed (3)• The
regulations on reduction of lead in leaded gasoline for health
reasons were reproposed because the Agency's basis for this
reduction was substantially revised and had not been available
for review by the scientific community.
At the time of the reproposal, the Agency was aware that
there had not been unanimity either within or outside the
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government with respect to the need to reduce lead in leaded
gasoline. In light of this controversy, the Agency requested
that informed and concerned members of the public provide EPA
with their opinions on the matter. This commentary was
encouraged by announcement in the Federal B§2i§t§£ (3) an<^
through approximately 150 individual letters specifically
requesting comments from members of the scientific and industrial
communities and from public interest groups.
As a result of these requests, numerous comments were
received by the Agency. Although a substantive response to each
comment was not possible, all comments were considered and are
available for public inspection at the Freedom of Information
Center of the Environmental Protection Agency in Washington, D.C.
The present paper is not intended as an encyclopedic
treatment of all that is known about lead. Rather, it is
intended tc be a presentation of the pertinent evidence upon
which a decision could be made as to whether or not there is a
health justification to regulate lead in gasoline. While the
emphasis in the paper is on lead as a gasoline additive, it has
been necessary to consider other sources of lead in the
environment in order to understand the role of leaded fuel in
relation to human lead exposure. The Agency has also considered
whether replacements for lead additives will result in
deleterious health effects to as great or greater degree than the
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lead additives themselves. This issue is discussed in a separate
paper entitled, "Lead in Gasoline, Impact of Pemoval on Current
and Future Automotive Emissions"
The present paper was prepared by a committee of EPA
scientists.
Members of the Committee Include:
John Buckley, Ph.D., Chairman
Kenneth Bridbord, MD Magnus Piscator, MD
Douglas I. Hammer, MD Lawrence Plumlee, MD
Robert Horton, MD Steven Reznek, Ph.D.
Marty Kanarek, MPH Richard Phoden, Ph.D.
Wellington Moore, DVM Jerry Stara, DVM
At least two committee members read and considered each of the
approximately 130 comments received on the reproposed regulation.
The results of this review process are reflected in the present
paper as is additional information which has become available
since reproposal of the regulation.
On October 1-2, 1973, EPA co-sponsored with the National
Institute of Environmental Health Sciences a Conference on Low
Level Lead Toxicity. A detailed evaluation of all presentations
at the Conference is beyond the scope of the present document.
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The proceedings from this Conference are due to be published in
the near future.
The present document is an extension of the earlier paper
entitled, "EPA's Position of the Health Effects of Airborne
Lead," dated November 29, 1972. At the time the earlier paper
was prepared, it seemed likely that catalytic converters would be
the principal means of reducing pollutants from automobiles for a
decade or more, and that the associated requirement of lead-free
gasoline to protect the catalysts would result in near-
elimination of automotive-related lead in the environment. It
now appears that the inrpact of catalytic converters may be more
transitory and that, unless regulated otherwise, lead additives
will continue to be used in substantial amounts. Thus the health
implications of leaded fuels become central to the regulatory
decision process.
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REFERENCES
1. Federal Register, Vol. 37, No 36; pp. 3882-3884, February 23,
1972.
2. Federal Register, Vol. 38, No. 6; pp. 1254-1256, January 10,
1973.
3. Federal Register, Vol. 38, No. 6; pp. 1258-1261, January 10,
1973.
4. Moran, J.B., "Lead in Gasoline, Impact of Removal on Current
Automotive Emissions." Environmental Protection Agency,
National Environmental Research center, Research Triangle
Park, North Carolina, October 1973.
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II. Occurrence and Sources of Lead in the Environment
Lead occurs naturally in the earth's crust and is also found
in the atmosphere and hydrosphere due to airborne dust, and to
gases diffusing from the earth's crust (1). Lead was one of the
first metals to be used by man, and evidence of the adverse
health effects caused by lead and its compounds is found in the
earliest annals of man's history. Deleterious effects from the
present use of lead can be a problem, particularly in certain
segments of the population. This Section will examine the
influence of man upon the distribution of lead in the
environment, especially with respect to the use of lead as a
gasoline additive.
Lead or its compounds may enter and contaminate the
environment at any step during the mining, smelting, processing,
and use of the metal and its derivatives. The annual increase in
lead consumption in the U.S. during the 10-year period 1962-1971
averaged 2.9%, resulting largely from an increased demand for
batteries and gasoline additives (2). During the same period,
lead used in pigments and caulking and in metal products
declined. In 1971 the total lead consumption was 1,431,514 short
tons with 596,797 short tons (H2%) coming from recycled lead
(3).
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Because lead and many lead salts or oxides are relatively
inert or immobile in the environment, a judgment can be made as
to the ease with which lead from various use categories can reach
and be transported through the environment. Table Il-l
summarizes lead consumption patterns in the United States for
1968 and 1971 (4,5) according to categories of environmental
impact. At this time, not all information required to compile a
detailed lead balance for the United States is available; thus
the above inventory of lead products in terms of their potential
release to the environment must be recognized as subjective.
As shown in Table II-l, 352,614 short tons or approximately
25% of the lead consumed in 1971 was in the form of metallic lead
or lead alloy. Most of this lead is chemically inert under
typical environmental conditions. As long as the size of the
piece of metallic lead or lead alloy is large, as is usually the
case within the metal products category, it is relatively
environmentally immobile. Recognized exceptions to this
generalization do exist and include small pellets of lead shot
often eaten by waterfowl, and the incineration of lead foils and
tubes, with resultant release of lead into the atmosphere.
Storage batteries accounted for 679,803 short tons of lead
consumption in 1971. This represents approximately 50% of the
total. Since a large fraction of the lead in storage batteries
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is recycled, little lead is believed to reach the environment
from disposal of storage batteries.
Lead is also commonly used as a coating material. In 1971,
some 53,198 short tons were in this category. Because of the
possibility of erosion or wear, the lead thus used must be
considered as potentially releasable into the environment.
More difficulty exists in classifying lead pigments in terms
of their potential for reaching the environment. Lead pigments
accounted for 81,258 short tons of lead consumption in 1971.
Much of this amount is tabulated simply as red or white lead or
litharge, rather than according to the actual category of use.
Based on shipping information, approximately one-fourth of the
lead classified under pigments in Table II-l is used in the
ceramics industry (6) and would thus have a relatively small
environmental impact. However, this form of lead could
contribute directly to human exposure through, for example,
improperly glazed dinnerware.
Lead pigment is used in printing inks and paints. Lead in
printer's ink, especially colored ink, has definite potential to
reach the environment as a result of incineration. The use of
lead-based paints in residential applications has been greatly
reduced in recent years, although the total used in the past is
still significant in terms of eventual environmental impact. The
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amount of lead released into the environment from pigments is
dependent on the relative quantity of waste disposal by
incineration compared to other disposal methods, as well as wear
and erosion of painted surfaces. On a national basis,
approximately 10-20% of all solid waste is incincerated (7).
This figure is assumed to be applicable as a first approximation
to estimate the release of lead to the environment from
incineration of lead pigments. The estimate does not necessarily
account for all lead incineration from demolished buildings,
since old paint tends to have a higher lead content. Further,
this does not reflect entrance of lead into the environment from
wear and erosion of exterior painted surfaces which has been
shewn to be substantial immediately adjacent to such surfaces.
(8)
In 1971, 264,240 short tons of lead consumed were in the form
of lead additives in gasoline. This amount is about one fifth of
the total consumption for that year. It can be calculated that
about 70% of the lead additives used in gasoline are emitted to
the environment as particulate matter from the tailpipe (9) .
Much of the balance remaining within the engine or exhaust system
of the vehicle is believed to eventually be removed from engine
surfaces by transfer to the oil or by flaking of deposits in the
exhaust system. The combustion of leaded gasoline accounts for
by far the largest portion of all lead now reaching the
environment, comprising about 90% of airborne lead emissions (9).
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As evidence of this contribution, a 43% reduction in lead
additives consumed within New York City during 1972 resulted in a
37% decrease in annual average ambient lead concentrations in the
city for 1972 compared to 1970-1971 (10). In a more detailed
calculation annual averages of air lead data from 38 sampling
sites across the city were as follows: July 1969-June 1970, 1.62
ug/m3; July 1970-June 1971, 1.71 ug/m3; and July 1972-June 1973,
1.18 pg/m . The latter figure reflects the decrease in air lead
following limitation of lead content of gasoline sold within the
city to 1.0 gram per gallon on January 1, 1972. Though
meteorologic differences from year to year, as well as sampling
and analytic variability could have accounted for some of this
decrease,the relatively constant city wide average in the two
years preceding reduction combined with the decline following
reduction make it evident that the contribution of lead additives
to airborne lead in New York City is substantial.
Table II-2 (9, 11, 12) summarizes the major discharges of
lead into the environment. Since current knowledge regarding the
mobility or activity of lead in the environment is incomplete,
the information in this table can only be regarded as semi-
quantitative. Of the total amount of lead found in the
atmosphere, the contribution from natural sources, such as the
re-entrainment of surface soil in the form of dust, is small.
3
This contribution has been estimated to be about 0.0005 pg/m of
air.(13) The lead concentrations in today's urban atmospheres are
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at least 100 to 1000 times greater than the amount which can be
attributed to natural sources.
As noted above, over two thirds of the lead added to gasoline
reaches the air environment (14). As lead leaves the exhaust
pipe of an automobile, initially all of it is airborne. The
heaviest particles fall to the ground within several hundred feet
of roadways, (15,16), whereas others remain suspended for longer
periods of time. The length of time that lead particles emitted
in auto exhaust remain airborne is determined primarily by
particle size and weight as well as by meteorological factors.
Lead is removed from the air by gravitational settling of larger
particles, aggregation and subsequent settling of smaller
particles, and through scavenging by various forms of
precipitation.
Fallout of automobile exhaust lead contributes to lead levels
found in dust and dirt which may in turn be resuspended in air.
Surveys of street and sidewalk dirt in Washington, D. C. and in
Boston showed lead concentrations commonly in the range of 1000
to 2500ug/g (ppm) with some values as high as 5000-10,OOOug/g
(17, 18). Samples of sidewalk dirt taken in the Bedford-
Stuyvesant area of Brooklyn, New York over a five month period
ranged from 900 to 4900 ppm lead (19).
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In a study of 77 midwestern cities, the average
concentrations of lead in dust collected at residential,
commercial, and industrial sites were 1,636 ug/g, 2413 ug/g, and
1512 ug/g respectively (20). Lead concentrations in surface soil
from three California city parks ranged from 194 to 3,357 ug/g
(21).
Lead levels in urban housedust commonly ranged from 1000-2000
ug/g in Boston (22) and averaged 500-900 ppm in Brattleboro,
Vermont, being higher in homes near roadways (23). In middle
class residential areas of New York City, lead in house dust
averaged 600-700 ug/g (2U) or 2-3 times higher than similar
measurements made in a suburban community. Lead emissions from
automobiles, and industrial sources, as well as weathering of
leaded paint all contribute to this contamination.
A very small part of the atmospheric lead resulting from lead
fuel additives is in an organic form (gaseous lead alkyls) .
Alkyl lead concentrations are rarely as high as 10% of ambient
air lead values (25, 26). Higher but transient peaks of alkyl
lead concentration have been demonstrated near specific sources
such as spills of gasoline containing lead alkyl compounds.
Air lead concentrations have been shown to be closely related
to the density of vehicular traffic, being highest in large
cities and progressively lower in the suburbs, smaller towns and
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rural areas (27). Data from non-urban sampling sites in the
National Air Surveillance Network (NASN) showed mean air lead
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concentrations of approximately 0.1-0.5ug/m during 1953-1966.
The mean concentrations at urban sites for those years were 1-
3ug/m .
In Pasadena and Los Angeles, air lead concentrations sampled
for two to seven hours have averaged from 9.4 to 23.6 ug/m^
3
during weekday traffic and have ranged up to 29.3 ug/m during
the morning rush hour (28) . Studies at different locations of
the Queens Midtown Tunnel and Triborough Bridge in New York City
showed that ambient lead levels averaged from 2.1 to 35.6 ug/m^
per 2U hours v»ith individual 24 hour peaks ranging up to 57.3
ug/m 3 (29) . About 68% to 88% of these airborne lead particulates
were in the respirable range.
One study has shown that air lead concentrations measured
during 1968-69 in Los Angeles, Philadelphia, and Cincinnati
increased 56%, 19%, and 17%, respectively, over concentrations
measured in 1961-62 (30). The average lead concentration
consistently increased at 17 of the 19 sampling sites and
meteorological conditions at each sampling site were consistent
for the two time periods. NASN data, which comes largely from
the central city commercial areas, does not show such a marked
increase during the same period, perhaps because traffic
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densities were consistently high in these areas in the 1961-1969
period.
The extent to which airborne lead has affected the lead
content of the earth's waters is difficult to ascertain. Lead
enters the aquatic systems through precipitation, lead dust
fallout and erosion and leaching of soil, as well as through
municipal and industrial waste discharges. In addition,
deposited lead (fallout) is washed off of streets, highways, and
other surfaces into rivers, lakes and marine waters.
Extrapolations from recent studies (31,32) indicate that on a
national basis the contribution of lead from fallout washing off
streets into water as urban runoff may be as high as 5,000 tons
each year. Tcday, surface waters in the Mediterranean and
Pacific Oceans contain up to 0.20 and 0.35 jag of lead/kg water
respectively, which is about 10 times greater than the estimated
pre-industrial lead content of marine water (33). The lead
content of rivers and lakes also has increased in recent
times.(33) A study of rainfall in various cities of the NASN
network indicated an average concentration of 36 ug of lead/liter
of rain which was approximately 40 times as high as that -found in
rainwater at non-urban sites (3U) .
Of concern is the possibility that continued contamination of
the environment by atmospheric lead has affected the
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concentrations of lead in biological systems and subsequently in
man's diet. Data suggest that some biological systems are
subjected to increased concentrations of lead in their
environment and certain portions of the food chain (earthworms)
have shown increases in lead content. (35). Shellfish that are
eaten by man are known to take up and store lead. Vertebrate
animals tend to store absorbed lead in bone rather than in flesh,
and therefore do not so readily transmit lead up the food chain.
The quantitative contribution of atmospheric lead to the food
chain of man is not known. Lead is a natural, although minor,
constituent of plants. Plants can absorb lead to varying degrees
(36). The solubility of lead is important when considering lead
uptake by plants. Experimental studies have shown that plants
can absorb and translocate only the soluble forms of lead (37).
There have been no reported observations that would indicate that
plants in the field are adversely affected by atmospheric lead.
The most important aspect of lead fallout on plants is the
potential hazard to humans or animals from the consumption of
contaminated and unwashed foliage, fruit or roots. In areas with
heavy lead dustfalls, such as along busy highways, substantial
amounts of lead are found on exposed surfaces of plants. Since
much of the atmospheric lead particulate is insoluble, a large
portion of the lead contamination remains on the surfaces of
plants. There is evidence of this source being important in lead
poisoning of grazing animals (38). To the extent that lead
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remains when plants are consumed by humans, it can add to man's
total body burden of lead.
Marine species, with the exception of shellfish, usually do
not concentrate lead from seawater and, hence, would not
contribute much to human lead exposure. In one study, eastern
oysters, soft-shelled clams, and northern quahogs were shown to
concentrate lead from seawater (39). Although concentrations of
lead reported in shellfish (range 0.17-2.5 ppm) are not high,
they do indicate the ability of certain edible aquatic species to
concentrate lead from the surrounding medium (40). Lead levels
in soft clams, hard clams, and surf clams have at times been
found that exceeded the maximum acceptable level proposed by
federal experts (41).
The World Health Organization reports that according to the
results of total diet studies in industrialized countries, the
total intake of lead from food generally ranges from 200-300 ug
per person per day. WHO further states that based upon available
data, these levels are similar to those found in the past 30-40
years and that no upward trend in lead levels in food is evident
(42).
Though lead in food would be the most consistent contributor
to total lead exposure for the general population, lead in food
is not the source that is most reduceable in the event that total
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exposure to lead is found -to be undesirable. For the general
population, "the lead in air is probably the contribution that is
most accessible to action for reducing the total body burden of
lead especially where this fraction is large compared with that
absorbed from food." (U3) Lead levels in food, of course, still
require careful monitoring to assure that excess exposure does
not occur from this source.
In conclusion, man made sources of lead contribute most to
the lead which enters the environment. Of these sources, the
combustion of leaded gasoline is the single most significant
contributor. Potentially, human exposure to environmental lead
may result from a number of sources, among them being the
inhalation of airborne lead and the ingestion of lead-
contaminated dusts. Reducing the amount of airborne lead in the
environment constitutes an accessible means for reducing
potential human exposure to environmental lead.
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TABLE II-l (4,5)
LEAD CONSUMPTION (SHORT TONS)
(UNITED STATES)
Product 1968 1971
Metal Products
Ammunition 82,193 87,567
Bearing metals 18,441 16,285
Brass & bronze 21,021 20,044
Cable covering 53,456 52,920
Casting metals 8,693 7,281
Collapsible tubes 9,310 10,041
Foil 6,114 4,417
Pipes, traps & bends 21,098 18,174
Sheet lead 28,271 27,607
Type metal 27,981 20,812
Weights & ballast 16,768 17,453
Solder 74.074 70.013
TOTAL 367,420 352,614
Storage Batteries
Grids & posts 250,129 322,236
Oxides 263,574 357,567
TOTAL 513,703 679,803
Coatings & Miscellaneous
Caulking lead 49,718 29,993
Annealing 4,194 4,068
Galvanizing 1,755 1,395
Plating 389 582
Terne metal 1,427 1,409
Other 17,924 15,751
TOTAL 75,407 53,198
Pigments
White lead 5,857 4,731
Red lead & litharge 86,480 61,838
Pigment colors 14,163 13,916
ZnO 3.234 773
TOTAL 109,734 81,258
Chemicals
Gasoline additives 261,895 264,240
Misc. chemicals 629 401
TOTAL 263,155 264,461
GRAND TOTAL 1,329,419 1,431,514
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TABLE II-2 (9, 11, 12)
LEAD EMISSIONS (TONS) TO THE ENVIRONMENT FOR 1968
(UNITED STATES)
Atmospheric
Gasoline combustion 181,000
Coal combustion 920
Lead alkyl manufacturing 810
Secondary smelting 811
Incineration of solid wastes 11,000
Other 755
TOTAL 195,316 I/
Water
Printing inks 10
Petroleum storage 24
Paint production 320
Battery production 600
TOTAL 954
Insecticides 2,081
GRAND TOTAL 198,351
!_/ It is estimated that 5,400 tons of lead due largely to automotive
lead emissions deposited on city streets reach the aquatic
environment. Additional, but unknown, amounts are washed out of
the atmosphere by precipitation and land directly on rivers, lakes
and marine water.
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REFERENCES
1. Airborne Lead in Perspective, A Report Prepared by the
Committee on Biological Effects of Atmospheric Pollutants,
National Research Council, National Academy of Sciences,
Washington, D. C., 1972, p.5.
2. Ryan, J.P., Minerals Yearbook 1971. U.S. Department of the
Interior. U.S. Government Printing Office, Washington, D.C.,
p. 671.
3. Ibid. , p. 684.
4. Ibid., p. 684.
5. Airborne Lead in Perspective, op.cit.; p. 11.
6. Ryan, J.P., op.cit., p. 686.
7. Klee, A.J., et.al., "Preliminary Data Analysis, 1968,
National Survey of Community Solid Waste Practices." USPHS
Publication #1867, Solid Waste Program, Cincinnati, Ohio.
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8. Comments submitted by the Ethyl Corporation to the
Environmental Protection Agency, March 9, 1973, pp. V-16 -
V-19.
9. Airborne Lead in Perspective, op.cit., pp. 11-13.
10. Personal communication from Fred C. Hart, Commissioner of Air
Resources, New York City, to William D. Ruckelshaus,
Administrator of EPA, March 20, 1973 and personal
communication from Edward F. Ferrand, NYC Department of Air
Resources to Kenneth Bridbord, EPA, Oct. 19, 1973.
11. "Recommended Methods of Reduction, Neutralization Recovery or
Disposal of Hazardous Waste," Prepared by TRW Systems Group,
EPA, Report f21485-6013-RU-OO, February 1, 1973, Vol. I, p.
92-94.
12. The Pesticide Review, 1972, U.S. Department of Agriculture,
Agriculture Stabilization and Conservation Service,
Washington, D. C.
13. Airborne Lead in Perspective, op.cit., p. 5.
14. Ibid., pp. 11-13.
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15. Motto, H.L., R.H. Dairies, D.M. Child, and C.K. Motto, Lead in
Soils and Plants. Its Relationship to Traffic Volume and
Proximity to Highways. Environ. Sci. Tech. 4:231-238, 1970.
16. Airborne Lead in Perspective, op.cit., p. 29.
17. Krueger, H.W., Krueger Enterprises, Cambridge, Mass.
Testimony submitted to EPA, July 10, 1972.
18. Fritsch, A., and M. Prival, Center for Science in the Public
Interest, Washington, D. C., Testimony submitted to EPA,
1972.
19. Lombardo, L.V., The Public Interest Campaign, Washington, D.
C., Personal Communication to Mr. William D. Ruckelshaus,
Administrator, U.S. Environmental Protection Agency, March 9,
1973.
20. Airborne Lead in Perspective, op.cit., p. 139.
21. Ibid, p. 30.
22. Krueger, H.W., op.cit.
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23. Darrow, D.K. and Schroeder, H.A., "Childhood Exposure to
Environmental Lead," paper presented before the American
Chemical Society, Chicago, 111., August 29, 1973.
21. Pinkerton, C., J.P. Creason, D.I, Hammer and A.V. Colucci,
"Multi-media Indices of Environmental Trace Metal Exposure in
Humans," presented at 2nd Int. Symp. on Trace Element
Metabolism in Animals, Madison, Wisconsin, June 1973.
25. Airborne Lead in Perspective, op.cit., p. 193.
26. U.S. Department of Health, Education and Welfare, Public
Health Service, Division of Air Pollution. Survey of Lead in
the Atmopshere of Three Urban Communities. PHS Pub. No.
999-AP-12. Cincinnati: Public Health Service, 1965. pp.
57-58.
27. Airborne Lead in Perspective, op.cit., pp. 18-21.
28. Ibid, p. 19.
29. Ferrand, E.F., Assistant Commissioner for Scientific Affairs,
New York City Department of Air Resources, Testimony
submitted to EPA April 11, 1972.
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30. Tepper, L.B. and Levin, L.S. A Survey of Air and Population
Lead Levels in Selected American Communities. Department of
Environmental Health, college of Medicine, University of
Cincinnati, Cincinnati, Ohio. Final Report (Contract PH-22-
68-28), December 1972. 73 pp.
31. Water Pollution Aspects of Street Surface Contaminants,
Environmental Protection Technology Series, EPA-R2-72-081,
November 1972, p. 3.
32. Environmental Pollution by Lead and Other Metals, NSF Rann
Grant 61-31605, University of Illinois at Urbana-Champaign
Progress Report May 1 - October 31, 1972, Chapter 6.
33. Airborne Lead in Perspective, op.cit., p. 6.
34. McCabe, L.J., J.M. Symons, R.D. Lee, and G.R. Robeck, Survey
of Community Water Supply Systems. J. Am. Water Works Assoc.
62(11): 670-687, 1970.
35. Gish, C.D. and R.B. Christensen, "Cadmium, Nickel, Lead and
Zinc in Earthworms from Roadside Soil", Environmental Science
and Technology, 7:1060-1062, November 1973.
36. Airborne Lead in Perspective, op.cit., p. 33-37.
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37. Ibid., pp. 33-37.
38. Ibid., FP- 178-182.
39. Pringle, E.H., D.E. Hissong, E.L. Katz, and S. Mulawka, Trace
Metal Accumulation by Estuarine Mollusks. J. Sanit. Eng.
Div.; Proc. Amer. Soc. Civil Eng. 94:455-475, 1968.
40. Airborne Lead in Perspective, op.cit., p. 189.
41. Metals in Shellfish with Particular Reference to Lead.
Prepared by the Northeast Water Supply Research Laboratory of
the U.S. Environmental Protection Agency, May 19, 1972, p.
17.
42. Joint FAO/WHO Expert Committee on Food Additives, Evaluation
of Certain Food Additives and the contaminants Mercury, Lead,
and Cadmium; WHO Technical Report Series, No. 505, 1972, p.
19.
43. Ibid., p. 20.
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Ill HEALTH ASPECTS OF LEAD EXPOSURE
It is apparent from our knowledge of the distribution of lead
in the geosphere and biosphere that lead in small amounts is a
natural part of living things. Lead enters animals from plants
which pick it up from the soil. In spite of its ubiquity, no
functional requirement for lead has been clearly demonstrated in
living organisms.
Because lead is easy to extract and purify, it ha? been used
for centuries. Lead, if improperly employed, is capable of
producing serious poisoning and even death. All of the
situations in which it is harmful are of human origin. For
example, no known cases of lead poisoning have originated from
natural amplification in the food chain. Much of our knowledge
of lead poisoning comes from occupational exposures to the me-'-al
or its compounds arid from ingest ion of lead by children.
The commonest symptoms of lead poisoning are anemia, severe
intestinal cramps, paralysis of nerves, particularly of the arms
and legs, and fatigue. The symptoms usually develop rather
slowly. High levels of exposure produce severe neurologic
damage, often manifested by encephalopathy and convulsions. Such
cases are frequently fatal. Today, severe cases of lead
poisoning in occupational situations are rarely seen due to
improved working conditions. Lead encephalopathy is now
predominantly found in young children who have consumed flakes of
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peeling lead paint, and also in some people who consume illegal
whiskey, which often contains lead.
Exposure to lead is usually assessed by means of lead levels
in blood and urine. Ordinarily, blood lead levels in the general
population are between 10 and 30 ug/ lOOg of whole blood. The
expressions "ug/lOOg of blood" and ug/ 100ml of blood" are for
all practical purposes equivalent and will be used
interchangeably in this paper, depending upon which is used in
the original references. Clinical symptoms of lead poisoning
usually do not appear until blood lead levels reach 80-100
ug/lOOg or higher. Symptomatic lead poisoning may, however, be
associated with blood lead levels in the range of 50-60 ug/lOOg
in instances where the patient's response to lead in the tissues
is modified as for example in the presence of anemia (1).
When the most severe effects of lead poisoning,
e.q.encephalopathy, have occurred and not been fatal, recovery is
frequently incomplete (2). Permanent, irreversible damage to the
nervous system often results, even though no further high level
exposure cccurs. With less severe effects such as anemia and
intestinal symptoms, residual, irreversible injury is not
observed if the exposure is discontinued. Recovery may be slow,
however.
Most injurious substances produce less conspicuous effects at
exposure levels somewhat below those resulting in overt symptoms.
III-2
-------
These less conspicuous effects must therefore be specifically
searched for by examinations or tests; otherwise, they may not be
observed. Lead is strongly suspected to produce such subtle
effects, but they have been much less well documented than have
the more conspicuous ones.
The suggestion that subtle lead effects occur comes in part
from studies of overt lead toxicity in which residual neurologic
effects were found during followup examinations among children
who initially were not deserved to have such symptoms. It should
be noted, however, that the problem of subclinical lead effects is
distinct from that of residual neurologic damage following lead
poisoning. Whether subclinical lead effects themselves can
result in residual neurologic damage is another question which
has not been adequately resolved.
In this regard, a study involving 425 children with lead
poisoning attributed primarily to ingestion of lead-based paint
found that 39% showed evidence of nervous system damage during
follow-up examinations (3). Mental retardation and recurrent
seizures were the most common and persistent findings. In many
instances neurologic symptoms were not found at initial
examinations. This study, however, dates back to 1955, when
diagnosis of lead poisoning often depended upon tests for urinary
coproporphyrins, which are not usually positive below 80-100 ug
of lead/100 g. whole blood. It is therefore probable that large
amounts of lead had been ingested. Extrapolation of these
III-3
-------
results tc children with blood lead levels below 80 ug/lOOg is
not appropriate.
Smith, et al (4) examined the neurologic sequelae in children
diagnosed with lead poisoning at least five years prior to study.
Permanent neurologic damage was found only in children who had
lead poisoning accompanied by encephalopathy. Subtle damage due
to lead exposure, however, could not have been recognized in this
study since sophisticated psychological and fine motor function
tests were not employed.
More recent studies have employed a greater degree of
sophistication in testing behavioral changes associated with
exposure to lead. Kotok et al (5) studied children with similar
socio-economic backgrounds to determine whether increased lead
body burden interferes with normal neurologic and motor
development. A group having a mean blood lead level of 81 ug/100
g was not found to differ significantly from a control group
having a mean blood lead of 38 ug/100 g. On this basis, it was
concluded that blood lead levels below those usually associated
with encephalopathy do not interfere with childhood development.
The mean blood lead level of the control group selected, however
indicated significant exposure to lead. Thus, firm conclusions
cannot be drawn from these data regarding whether or not lead
adversely affects the nervous system at blood lead levels of
80ug/100g or below.
III-4
-------
Albert, et al. (33) employed psychological tests, medical
examinations, nerve conduction studies and school records to
evaluate whether deleterious effects could be associated with
childhood lead exposure below overt toxicity. Excess lead
exposure was measured in terms of lead levels in teeth. In the
absence of a diagnosis of lead poisoning or a blood lead level in
excess of 60 pg/lOOg, high levels of lead in teeth were not
associated with deleterious health effects. In constrast,
adverse effects were seen in children with blood lead levels in
excess of 60 ug/lOOg who received no chelation therapy as well as
among these who were treated for severe lead poisoning.
A. study by Pueschel et.al. (6) suggests that in children lead
body burdens below those usually associated with clinical
poisoning contribute to renal as well as neurological damage.
Fifty-eight children between the aqes of 6 months and 6 years
were selected for study from a larger sample of children living
in a high-risk lead poisoning area. The majority of these
children were known to ingest paint and dirt. The children
examined had blood leads over 50 ug/lOOml or had blood leads over
40 jag/lOOml with urine leads exceeding 500 ug/2U hours following
EDTA provocation.
While most of the children did not exhibit symptoms uniquely
attributable to lead poisoning, over one-third were found to have
a history of mild CNS symptoms. The symptoms were observed
significantly more frequently in these children than in a matched
control group. Subsequent follow-up study revealed that many of
Hl-5
-------
the children examined still had behavioral and school
diff icxilties, even though sources of lead exposure had been
removed in most cases. Since complete data on the control groups
were not presented, it is difficult to fully evaluate the
significance of these findings.
Of particular interest in Pueschel's work is the observation
of anemia, aminoaciduria, proteinauria, and casts in a high
percentage of the children. It may be noted that studies by
Betts, et. al. suggest anemia can occur in children with blood
lead levels between 37-60 ug/lOOml and studies by Tola, et al.
found mild anemia occurring in lead workers with blood leads
between 40-60 ug/lOOg (7-8) . Although factors such as
nutritional status and deprived environments may have been
responsible for the anemia and renal and neurological damage-
observed by Pueschel, these effects are consistent with damage
that has been related to lead exposure.
It has teen suggested by David, et al. (1) that- childhood
behavioral disturbances such as hyperact ivity may be associated
with blood lead levels between 25-55 ng/lOOrnl. About half of r!v
hyperactive group studied (28 of 5U) had blood leads between 2r™
5S ug/ 100ml compared to less than one third (10 of 37) in the
control group. Both the hyperactive arid the control groups w^re
similar with respect to age and sex, but socio-economic, racial
and dietary differences between the groups may have confounded
the results. Further, the children studied for hyperactivity may
have had much higher lead absorption at an earlier age with a
III-6
-------
subsequent decline in blood lead level by the time of study.
Because the hyperactive child is more likely to have pica
(abnormal ingestion of non-food substances), it is possible that
the hyperactivity caused the increased lead intake rather than
having been the consequence of it. The David study suggests,
although it does not prove, that exposure to lead in quantities
not generally considered excessive or toxic may contribute to
hyperactivity in children. Additional studies are necessary to
define the relationship between hyperactivity and causal factors,
including lead. Studies by Silberqeld, et al. (34) may be
important in this regard. Mice exposed to high levels of lead
from birth developed hyperactivity which, as in children with
this disorder, responded atypically to CNS stimulants and
depressants.
A study by de la Burde, et al. (10) concluded that children
ingesting paint or plaster containing lead are more likely to
have abnormal or suspect behavior and fine motor disabilities
than children not so exposed. Subjects in this investigation
were followed prospectively and were selected to eliminate pre-
existing neurologic abnormalities. The lead-exposed group had a
mean blood lead level of 58 ug/100 g (range 40 to 100 ug/lOOg);
blood leads were not measured in the controls. Lead intake
differences between the groups were established on the basis of
measures cf urinary coproporphyrins.
Results indicate that the control group performed better than
the exposed group in the areas tested. Most notable differences
III-7
-------
were with respect to fine motor ability and behavior. These
results, however, may have been confounded by the failure to
measure blood leads in the controls and by the failure to
exclude, in the exposed group relative to the controls, an
increased incidence of pica. Increased behavioral deficiencies
observed in the exposed group could have been related to a
greater frequency of pica in this group rather than the ingestion
of lead per se.
Some studies have recently been undertaken to determine the
lowest exposure levels at which lead-induced injury to the
peripheral nerves can be detected (11-13). One study shows that
in adults disturbances in conduction velocity can be found at
blood lead levels of 80 ug/lOOg and above. Preliminary results
also noted in this study indicate the presence of mild neuropathy
in lead workers at blood lead levels under 50 ug/100 g (13).
The potential problem of subclinical neurological damage
caused by lead is an important one which deserves further
attention. Whether subtle adverse effects on CNS function such
as small decreases in IQ, interference with fine motor function
and altered behavior can be attributed to lead exposure is still
uncertain. If such effects do occur they may be related to a
degree of exposure less than that recognized as producing overt
lead poisoning.
In recent years evidence has been accumulated that
significant exposure to lead will produce injury involving the
III-8
-------
kidneys and other organ systems. This knowledge of complex and
varied effects has recently been reviewed by the National Academy
of Sciences (NAS). Table III-l which is reproduced here from
Table 1-11 of the NAS review of lead displays a detailed outline
of effects at various exposure levels (14) . It should be noted
that some of these effects are more typically associated with
lead exposure in children than in adults.
Because anemia is an evidence of lead toxicity, blood and
blood cell formation have been studied particularly for early
changes; shortened red cell life span (15) and lowered hemoglobin
(16) have teen observed. Injury to enzyme systems involved with
the formation of hemoglobin has also been observed, but, because
some of these systems are disturbed by substances and conditions
other than lead, the observations are difficult to interpret.
One biochemical change, indicated by an increased urinary
excretion of delta aminolevulinic acid (ALA-U), is of particular
interest because it is rarely produced by anything other than
lead (17). This increase in ALA-U is one of the most thoroughly
studied of the metabolic alterations produced by lead. It is
directly related to inhibition of the enzyme delta-aminolevulinic
acid dehydrase (ALAD) which converts ALA to porphobilinogen.
Elevated ALA-U has been shown to be closely related to elevated
lead levels in the soft tissues and may reflect biochemical
changes in these tissues (18-19). Soft tissue lead is considered
to be the metabolically active portion of the body lead burden.
III-9
-------
(20) For these reasons, increased ALA-U is considered to be an
undesirable change indicative of probable health risk (21).
The appearance of excess ALA in the urine is first seen at
blood lead levels of 40-60 ug/100g (22-25) . If increased urinary
ALA excretion is undesirable, it then follows that blood lead
levels above 40 jig/IOOg are to be avoided, if possible. In this
context, the National Academy of Sciences Lead Panel concluded
(26), "...the exponential increase in ALA excretion associated
with blood lead content above approximately 40 ug/100g of blood
signifies inhibition of ALAD that is physiologically significant
in vivo."
Recent animal experiments, using graded levels of lead
exposure, show beginning injury to kidneys at about the same
exposure level as that causing increased ALA-U excretion (27).
While these kidney changes are probably reversible when mild, it
is known that permanent damage to the kidneys results from higher
doses of lead (28). The degree and duration of exposure needed
to produce irreversible changes are not known, although it is
unlikely that they could be caused solely by lead in the ambient
air.
Animal studies indicate that lead at much higher dosages than
man would generally be exposed to is capable of disturbing the
biological defense mechanisms that provide protection from
bacterial and viral infection (29-31). The mechanism by which
lead aggravates viral disease is by reduced interferon synthesis
111-10
-------
rather than by inhibition of interferon action (32). Because it
has become apparent that lead may produce this type of injury,
further studies, with expected exposure routes and realistic
exposure levels, should be of considerable interest.
The studies reviewed in this Section permit no unequivocal
conclusions to be drawn. On balance, the studies suggest that
subclinical changes may be associated with blood lead levels in
the range cf UO-60 ug/lOOg. As blood lead levels increase above
40 ug/lOOg, the likelihood that significant changes will occur
increases markedly. Based upon evidence from these studies, it
would seem prudent to regard blood lead levels over UO ug/lOOg as
indicators of lead intake that should be prevented. The 40
ug/lOOg figure, however, does not represent a sharp demarcation
between health and disease.
III-ll
-------
TABLE III-l (14)
TABLE 4- 1 1 Level and Types of Effects
and Remote
Level I:
No Demonstrable
Type of Effects in vivo Effect
Metabolic (accumu- Changing
lation and excte- A LAD"
tion of he me
precursors)
Functional injury:
Hematopoiesis None
Kidney (renal None
tubular
function)
Central nervous None
system
Peripheral None
nerves
Clinical effects None
Index of level of
recent or
current ab-
sorption:
Blood lead, <40
ug/100gof
whole
blood
Urine lead —
(adults only),
fig/liter
of Inorganic Lead Salts as Related to Est
Level II:
Minimal Level 111:
Subchnical compensatory tsioiogic
Metabolic Effect Mechanisms Invoked
Slight increase in ALA, UCP, FEP
urinary ALA progressively increased
, may be
present
None known Shortened red-cell life-
span, reticulocy-
tosis (±)
(reversible)
None known ?
None known ?
None known ?
None known Nonspecific mild symp-
toms (may be due
in part to coexist-
ing diseases)
40-60 50-100+
<80 <130
.
imates of Various Levels ot
Level IV:
Acute Lead Poisoning
MUd Severe
ALA, UCP, FEP
increased 5- to 100 fold
Shortened red-cell life-span
and reticulocytosis
with or without anemia
(reversible)
Amino- Fanconi
aciduria, syn-
glycosuria drome
(±) (re- (revers-
versible) ible)
Mild injury Severe injury
(??? re- (perma-
versible) nent)
Rare Rare
Colic, irri- Ataxia, stu-
tability, por, coma,
vomiting convulsions
>80 >80
With anemia,
intercurrent disease:
50-100+
>130 >130
(May be less in severe illness)
Absorption-Recent
Level V:
Late Effects of
Chronic or Recur-
rent Acute Lead
Poisoning
Increased if exccwivc
exposure rcccm .
but may not be n-
creasedif exce-.Mvc
exposure termite
Anemia (t)
(reversible)
Chronic nephropjtl'v "
(permanent)
Severe injury6
(permanent)
Impaired conduction
(wrist, foot drop
usually improve
slowly, but may be
permanent)
Mental deficiency
(may be profound).
seizure disorder.
renal insufficiency
(gout) (perma-
nent)
May be normal
Spontaneous
excretion may be
normal
"See p. 106 for discussion of changing levels of ALAD.
CaEDTA mobilization test in chronic nephropathy is positive; may or may not be positive in permanent central nervous system injury.
-------
REFERENCES
1. "Airborne Lead in Perspective," Report prepared by the
Committee on Biologic Effects of Atmospheric Pollutants,
National Research Council, National Academy of Sciences,
Washington, B.C., 1972, p. 130
2. "Airborne Lead in Perspective," op. cit., p. 95
3. Perlstein, M.A., and R. Attala, "Neurologic Sequelae of
Plumbism in Children Clin. Ped. 5:292-298, 1966
4. Smith, H.D., Baehner, R.A., Carney, T. and Majors, W.J., "The
Sequelae cf Pica With and Without Lead Poisoning." Amer.
Jour. Cis Child. 105: 609, 1963
5. Kotok, C., Development of Children with elevated blood lead
levels, Prediat. 80: pp. 57-61, Jan 1972
6. Pueschel, S.M., Kopito, L, and Sohwachman, H., Children with
an increased lead burden, Jour. Amer. Med. Assoc. 222:4:462-
466, Oct. 23, 1972
7. Betts, P.R., Ashley R. and Raine, D.N., "Lead Intoxication in
Children in Birmingham,"Brit. Med. Jour., l:pp. 402-406, 1973
8. Tola, S., Hernberg, S., Asp, S., and Nikkanen, J.,
"Parameters Indicative of Absorption and Biological Effect in
New Lead Exposure: A Prospective Study," Brt. J. of Ind.
Med., 30: pp. 134-141
9. David, O., Clark, J. and Vohller, K., "Lead and
hyperactivity" Lancet, 2: 900-903, October 28, 1972
10. de la Eurde, B., and M.S. Choate, Does asymptomatic lead
exposure in children have latent sequelae? Pediat.
81:6:1088-1091, December 1972.
11. Catton, M.J., G. Harrison, P.M. Fullerton and G. Hazantzis,
Subclinical neuropathy in lead workers, Brit. Med. Journ. 2:
80-82, 1970.
12. Seppalainen, A.M. and S. Hernberg, Sensitive technique for
detecting subclinical lead neuropathy, Brit. Journ. Indust.
Med. 29: 443-449, 1972.
13. Hernberg, S., Biological effects of low lead doses, Proc.
Int. Symp. Envir. Hlth. Aspects Lead, CED, CID, pp. 617-629,
Luxembourg, May 1973.
111-12
-------
14. Airborne Lead in Perspective, op. cit., pp. 128-129.
15. Hernberg, S, M. Nurminen and J. Hasan, Nonrandom shortening
of red cell survival times in men exposed to lead, Environ.
Res. 1:247-261, 1967.
16. Williams, M.K., Blood lead and hemoglobin in lead absorption,
Brit. Jcurn. Indust. Med. 23:105-111, April 1966.
17. Airborne Lead in Perspective, op. cit., p. 106.
18. Cramer, K. and S. Selander, Studies in lead poisoning:
Comparison of different laboratory tests, Brit. Jour.
Indust. Med. 22: 311-314, 1965.
19. Selander, S., K. Cramer and L. Hallberg, Studies in lead
poisoning: oral therapy with penicillamine. Relationship
between lead in blood and other laboratory tests, Brit.
Journ. Indust. Med. 23: 282-291, 1966.
20. Airborne Lead in Perspective, op. cit., p. 123.
21. Airborne Lead in Perspective, op. cit., p. 132.
22. Selander S. and K. Cramer, Interrelationships between lead in
blood, lead in urine, and ALA in urine during lead work,
Brit. Jour. Indust. Med. 27: 28-39, 1970.
23. Hernberg, S, J. Nikkanen, G. Mellin and H. Lilius, Delta-
aminolevulinic acid dehydrase as a measure of lead exposure,
Arch. Envir. Hlth. 21:140-145, 1970.
24. Tola, S., The effect of blood lead concentration, age, sex,
and time of exposure upon erythrocyte deltaaminolevulinic
acid dehydrase activity, Work Envir. Hlth. 10: 26-35, 1973.
25. Tola, S., S. Hernberg, S. Asp and J. Nikkanen, "Parameters
indicative of absorption and biological effect in new lead
exposure: a prospective study," Brit. J. Ind. Med., 30: pp.
134-141, 1973.
26. Airborne Lead in Perspective, op. cit., p. 110.
27. Goyer, R.A., J.F. Moore and M.R. Krigman, Lead dosage and the
role of the intranuclear inclusion body. Arch. Envir. Hlth.
20: 705-711, 1970.
28. Airborne Lead in Perspective, op. cit., p. 131.
29. Selye, H., B. Tuchweber and L. Bertok, Effect of lead acetate
on the susceptibility of rats to bacterial endotoxins, Journ.
Bacteriol., 91: 884-890, 1966.
111-13
-------
30. Hemphill, F.E., M.A. Kaeberle and W.B. Buck, Lead suppression
of mouse resistance to Salmonella typhimurium, Science 127:
1031-1032, June 4, 1971.
31. Gainer, J.H., "Effects of Metals on Viral Infections in
Mice," Env. Health Persp., pp. 98-99, June 1973.
32. Gainer, J.H., "Lead Aggravates Experimental Viral Infections
and Represses the Antiviral Activity of Interferon Inducers,"
paper presented at EPA-NIEHS Conference on Low Level Lead
Toxicity, Raleigh, N.C., Oct. 1-2, 1973.
33. Albert, R.E., R.E. Shore, A.J. Sayers, C. Strehlow, T.J.
Knelp, B.S. Pasternak, A.J. Friedhoff and J. Goodgold,
"Followup of Children Overexposed to Lead," paper presented
at EPA-NIEHS Conference on Low Level Lead Toxicity, Raleigh,
N.C. , Oct. 1-2, 1973.
3U. Silbergeld, E.K. and A.M. Goldberg, "Hyperactivity: A Lead-
Induced Behavior Disorder," paper presented at EPA-NIEHS
Conference on Low Level Lead Toxicity, Raleigh, N.C., Oct. 1-
2, 1973.
111-14
-------
IV. Canaan AccgBtable_Lead^Body^Burden be^Defined?
In Section III the spectrum of effects due to lead was
reviewed with special emphasis upon subclinical changes believed
to be of health significance. This Section will examine how
these findings may be of assistance in helping to define an
acceptable lead body burden for the general population.
Exposure to toxic substances is difficult to quantify with
external measurements, especially when exposure may occur via
food, water and air. It is preferable, if possible, to measure
an integrated index of these exposures within the body. The
blood level of lead which itself is not an adverse health effect
serves as such an index, and, under most circumstances is a
reasonably accurate measure widely employed in public health
surveillance. This measurement serves not only as an index of
continuous lead exposure, but also as a diagnostic tool in
identifying cases of lead poisoning and undue lead absorption.
Due to the ubiquitous nature of lead, the general population
carries blood lead levels of 10-30pg/100g. As exposure
increases, blood lead levels rise, although slowly and in a
nonlinear fashion, because excretion of lead also rises with
increasing exposure. Thus blood lead levels are a satisfactory
index of soft tissue lead burden during constant exposures, but
-------
are less accurate during rapid changes in lead exposure or in
total body burden.
Blood lead concentration is the net result of several
independent equilibria. Accordingly a single blood lead
determination will not necessarily indicate a high nor exclude a
low body burden of lead. Serial determinations are therefore
recommended to assure the validity of the initial value as well
as to ascertain rates of change (1). The variability of
laboratory methodology and accuracy is also often considerable,
and the confidence limits of the analytical procedure must be
taken into account especially when comparing results among
different laboratories.
Although physicians are generally well aware of limitations
with the use of blood lead levels, the even greater variability
of other indices and the ease of obtaining blood specimens make
determination of blood lead the single most useful parameter.
Other indices are helpful, including: concentration of lead in
urine, feces, and hair; ALA in the urine; urinary coproporphyrin;
erythrocyte delta aminolevulinic acid dehydrase, protoporphyrin,
basophilic stippling, and red cell survival time; hemoglobin; and
hematocrit. A detailed discussion of the relative merits of
these techniques is beyond the scope of the present paper.
IV-2
-------
As noted in Section III, blood lead levels of 40ug/100g and
above have been associated with subclinical changes as well as
increased lead body burdens, and as such are considered to be
evidence that significant lead intake has occurred. This 40
ng/100g level has been accepted as evidence of undue exposure to
lead in children and adults (2,3,4), although one must recognize
that this level does not represent a sharp demarcation between
health and disease.
The U.S. Public Health Service has recommended (3) that, for
older children and adults, until proven otherwise by additional
research, "... a blood lead concentration of UOug or more per
100ml of whole blood, determined on two separate
occasions, be considered evidence suggestive of undue absorption
of lead, either past or present." This recommendation also
established 80ug/100ml whole blood as unequivocal lead poisoning
and 50-79ug/100ml as requiring immediate evaluation as a
potential poisoning case.
The FEP test (free erythrocyte protoporphyrins test)
developed by Piomelli et al (11), shows promise of identifying
the presence of undue metabolic effects resulting from lead
exposure. The FEP test is capable of detecting an interference
in heme synthesis caused by lead in the bone marrow. This
interference, if present to a significant degree, could reflect a
degree of lead exposure associated with toxic metabolic effects.
IV-3
-------
The FEP -test is especially valuable since it is well recognized
that blood lead levels do not, in themselves, constitute an
absolute criterion of lead effect.
There exists debate within the scientific community with
respect to what concentration of FEP in the blood constitutes an
abnormal elevation. As originally proposed by Piomelli, an FEP
level of 250 ug/lOOml of RBC appeared a reasonable upper limit
above which significant adverse effects due to lead were likely
occurring. This 250 ug/lOOml cutoff is approximately three times
the FEP level found in 1-6 year old children with blood leads
under 20 pg/lOOml. There are, however, scientists who advocate a
lower FEP cutoff to provide a greater margin of safety in any
screening program.
Piomelli found that all children studied with blood leads of
60 ug/lOOml or above had FEP levels in excess of 250 ug/100 ml of
RBC. Among children with blood lead levels between 40-59
ug/lOOml, 55% were observed to have FEP levels above 250
ug/lOOml. In contract, only 5% of children with blood leads
below 40 pg/lOOml had elevated FEP levels. In this regard, one
must consider the possibility that iron deficiency anemia
potentiates lead toxicity even at blood lead levels below UO
ug/lOOg (12). The widespread prevalence of iron deficiency
anemia among the population at greatest risk from lead exposure
should also be noted. A positive FEP test accompanied by a blood
IV-4
-------
lead below HO ug/lOOml urually reflects the presence of iron
deficiency anemia although this could also be an early indicator
of undue lead absorption. The finding that 55% of children with
blood leads between 40-59 ug/lOOml have elevated FEP levels,
combined with the exponential increase in FEP observed at blood
leads above 40 ug/lOOml, suggests the more frequent occurrence of
adverse metabolic effects among children whose blood leads have
risen to 40 ug/lOOml and above. Combined with blood lead
determinations, the FEP test would provide a more objective
evaluation of lead toxicity than possible by either test alone.
It may well be that subclinical neurological effects due to lead
are more closely related to FEP levels in the hematopoietic
system than to isolated measures of blood lead (13).
Environmental insults may put certain population subgroups
such as children, the aged or infirm, and pregnant women at
greatest risk. Although there is no clear evidence of increased
susceptibility to lead in children, they may be considered a
potentially high risk group because they have greater opportunity
to ingest lead from environmental sources such as paint, dust or
dirt. High lead exposure gives rise to renal tubular damage in
children, which is an unusual consequence in adults. In
children, excessive exposure is frequently associated with sudden
onset of encephalopathy which is often followed by permanent
brain damage (5). The onset of encephalopathy without previous
symptoms is uncommon in adults.
IV-5
-------
Angle and Mclntire (6) concluded that, there is a definite
fetal risk, maximal in the first trimester, from intrauterine
exposure to high concentrations of lead in maternal blood.
Studies by Kochen and Haas et al (7,8) confirm that umbilical
blood lead concentrations are similar to those in maternal blood.
In the newborn the blood-brain barrier is relatively immature
(9,10) and the mass of central nervous system tissue is greater,
while the mass of skeletal tissue is less, per unit of body
weight. With the well documented neurotoxicity of lead, it is
clear that additional data are necessary to evaluate the
possibility of increased susceptibility to lead exposure in the
fetus and neonate.
Two recent experiments are suggestive of a special
susceptibility to lead among animals exposed either prenatally or
during infancy. In one instance (14) , lambs exposed to maternal
blood lead levels of 34 ug/lOOml during gestation demonstrated
slowed learning on a visual discrimination task at 10-15 months
of aqe. This deficit is consistent with visual-perceptual
problems that have been noted in children with lead poisoninq.
Extrapolation of these findings directly to man is, however,
somewhat uncertain since a blood lead of 34 ug/lOOml in sheep may
be equivalent to a higher blood lead in man. In another instance
(15), infant rhesus monkeys fed 0.5 mg lead acetate per kg of
body weight developed hyperactivity and insomnia. Blood leads in
these infant monkeys ranged from 60-100 ug/lOOml. In contrast
IV-6
-------
the physical status and behavioral status was unchanged in
juvenile monkeys fed lead acetate at 20 mg/kg sufficient to
produce average blood leads of 135 ug/lOOml. Though lead dosages
administered to the monkeys were well in excess of those found in
human lead poisoning, the dependence of response upon age is
noteworthy.
It is not possible at this time to firmly establish a single
acceptable blood lead level protective of all high risk
population subgroups. It would appear prudent, however, to
recommend that the current U.S. Public Health Service guideline
for older children and adults, i.e., UOug/lOOml whole blood, be
regarded as a strict upper limit for younger children. Whether
the acceptable upper limit should be lower than UOug/lOOml for
the fetus, neonate, and the woman of child bearing age will
require further investigation.
Important questions that necessitate additional study to help
define with greater confidence an acceptable lead body burden
include the following:
(1) At what level of exposure or body burden do effects of
lead become irreversible?
(2) Are some of the permanent effects not immediately
recognizable, especially in children?
IV-7
-------
(3) When the less severe effects subside is there no
residual, or are there some permanent changes which are
not noticeable?
(U) What combinations of level and duration of exposure
prcduce irreversible lead poisoning?
(5) Does injury to other organs or systems such as the liver
or biological defense mechanisms occur at levels of
exposure and lead body burden common among the general
population?
(6) At what level of exposure and lead body burden are
changes due to lead found which produce no symptoms and
will such changes if long continued produce irreversible
damage?
(7) Which groups among the general population are most
sensitive to lead and which factors can significantly
affect lead toxicity?
Considerably more research is thus necessary to clarify these
as well as other incompletely answered questions related to lead.
IV-8
-------
REFERENCES
1. Lin Fu, J.S., "Undue Absorption of Lead among Children -
A New Look at an Old Problem," N. Eng. J. Med., 286 (13),
702-710, 1972.
2. "Airborne Lead in Perspective," report prepared by
the Committee on Biological Effects of Atmospheric
Pollutants, Division of Medical Sciences, National
Research Council, National Academy of Sciences,
Washington, B.C. 1972, pp. 100-110
3. "Medical Aspects of Childhood Lead Poisoning," HSMHA
Health Reports, 86(2), 140-143, 1971
4. Chisolm, J.J., Baltimore City Hospitals, in testimony
submitted to EPA, July 26, 1972.
5. Lin Fu, J.S., op cit.
6. Angle, C.R., and M.S. Mclntire, "Lead Poisoning During
Pregnancy," Amer. J. Dis. Child., 103, 436-439, 1964.
7. Kochen, J.A., Mentifiore Hospital and Medical Center,
IV-9
-------
personal communication to K. Bridbord, EPA, April 18, 1973.
8. Haas, T.; K. Mache; K. Schaller; A. Wieck; W. Mache; and
H. Valentin; "Untersuchungen Uber Die Okologishe
Bleibelastung Im Kindesalter;" Proceedings of the
International Symposium on the Environmental Health Aspects
Lead, CEC, CID, Luxembourg, May, 1973, pp. 741-748.
9. Bobbing, J.: The development of the blood brain barrier
Prog. Br. Res. 29: 417-27, 1968
10. Evans, C.A. et al.: The development of blood brain
barrier and choroid plexus function in immature
foetal sheep, J. Physiol 224:15-16, July 1972
IV-10
-------
11. Piomelli, S.r B. Davidow, V. F. Guinea, P. Young and
G. Gay, The FEP (Free Erythrocyte Protoporphyrins)
Test: A screening Micromethod for Lead Poisoning,
Pediatrics, 51:254-259. February 1973, and Letters
to the Editor, Pediatrics 51:303-306. March 1973.
12. Angle, C. R., and M. S. Mclntire, "Red Cell Lead,
Whole Blood Lead and Red Cell Enzymes," Paper presented
at EPA-NIEHS Conference on Low Level Lead Toxicity,
Raleigh, North Carolina, October 1-2, 1973.
13. Chisolm, MM., D. Mellits, J. E. Keil and M. B.
Barrett, Variations in Hematologic Responses to
Increased Lead Absorption in Young Children, paper
presented at EPA-NIEHS Conference on Low Level Lead
Toxicity, Raleigh, North Carolina, October 1-2, 1973.
14. Carson, T. L., G. A. Van Gelder, G. G. Karas and W. B.
Buck, Development of Behavioral Tests for the Assessment
of Neurologic Effects of Lead in Sheep," paper presented
at EPA-NIEHS Conference on Low Level Lead Toxicity,
Raleigh, North Carolina, October 1-2, 1973.
15. Allen, J. R., P. J. McWey and S. J. Suomi, "Pathobiological
iv-n
-------
and Behavioral Effects of Lead Intoxication in the Infant
Rhesus Monkey," paper presented at EPA-NIEHS Conference on
Low Level Lead Toxicity, Raleigh, North Carolina, October 1-
2, 1973.
IV-12
-------
V. Relationship of Environmental Lead Exposure to Human Lead
Intake
In Section II it was demonstrated that lead emitted from
motor vehicles reaches the environment in substantial quanities
by several routes including lead suspended in air and fallout of
lead into dust and onto soils. This widespread dispersal of lead
into the environment resulting from the presence of lead in
gasoline, may contribute to man1s intake of lead. The routes of
intake of lead into man from the environment are through ingested
food and non-food items, water, dust, and air inhalation. This
present Section examines the extent to which man's lead intake
could be affected by lead emissions from motor vehicles and what
effect, if any, this may have upon the people so exposed.
Lead is added to gasoline as tetraethyl lead, an organic
compound. Exposure to organic lead is dangerous and an important
occupational health problem. As indicated in Section II, a very
small part of the atmospheric lead resulting from fuel additives
is in an organic form (gaseous lead alkyls) and there is little
opportunity for general population exposure. General population
exposure is much more likely to come from inorganic lead
contained in the aerosol particulate emitted from automobiles.
-------
To more fully understand the factors affecting man's lead
intake and any resulting biomedical effects, it is useful to
discuss the routes of lead absorption, the quantity of lead
available through each route, and the differential absorption
among the various routes. It is in this context that the sources
of lead intake can be examined with respect to the highest amount
of total daily lead intake that is generally considered safe or
acceptable over a long period of time. For the general
population, absorption of lead through the skin is nil. The lead
that is swallowed into the gastrointestinal tract is available
for absorption regardless of source, but only a small portion is
actually absorbed. Similarly, lead inhaled into the respiratory
tract is available for absorption through the lungs or from the
gastrointestinal tract after it has been moved to the throat by
ciliary action and subsequently swallowed. Only a portion of the
inhaled lead is absorbed.
Commonly accepted figures for daily dietary lead intake in
adults are on the order of 200-300 ug/day with ranges of 100-500
ug/day (1, 2). Gastrointestinal absorption of lead is primarily
a function of the chemical composition of the diet and is usually
estimated to be 10%, although it has been reported to be lower in
adults (3, U). Young children, however, may absorb considerably
more lead, up to 50% of their oral lead intake (5). Recent
experiments in animals indicate that diets low in calcium
greatly increase lead absorption from the gastrointestinal tract
V-2
-------
and affect lead distribution in the body with more lead being
stored in the soft tissues (6). Diets low in calcium and low in
iron have both been shown to increase lead toxicity in rats fed
subtoxic quantities of lead in drinking water (7).
Respiratory absorption of lead is dependent upon the size,
shape, and density of the inhaled particles as well as the rate
and volume of respiration. For respiratory absorption, 30% is a
commonly accepted figure, assuming essentially complete pulmonary
retention of deposited lead particles of the size found in
ambient air. (8) Other estimates of respiratory lead absorption
have ranged from 17% to 37% (9, 10). Thus, for equal amounts of
available lead, an average of about three times as much of a
given amount of lead would be absorbed from the respiratory tract
as from the gastrointestinal tract. Table V-l summarizes the
results of EPA's calculations to estimate the contribution of
airborne lead to total daily lead absorption among adults in the
general population. A lead isotope tracer technique developed by
Rabinowitz et al. has been helpful in further clarifying the
relative contribution made by airborne lead to total lead
absorption in man (11) . Preliminary results from these isotope
studies are consistent with the calculations in Table V-l.
Since, as noted in Section II, lead in gasoline is by far the
largest contributor to airborne lead, the calculations in Table
V-l indicate that lead in gasoline can make a substantial
contribution to lead absorption in man.
V-3
-------
In the classic experiments which he summarized in the 1960
Harben lectures, Kehoe fed known amounts of lead to four subjects
and monitored their daily intake and output of lead as well as
the lead concentrations in their blood and urine. (12) Each
subject had a daily diet containing about 300 ug of lead to which
additional lead was added in the following quantities:
approximately 300 ug (Subject S. W. ) , 1000 ug (Subject M. R.),
2000 ug ( Subject E. B. ), and 3000 ug (Subject I. F.). The
average daily total intake for each study subject was 600 ug,
1270 ug, 2350 ug, and 3270 ug respectively. Gastrointestinal
absorption was determined to be about 10% of the dietary lead
dose. In his Harben lectures, Kehoe plotted the average blood
lead level for each subject for consecutive 28-day periods during
the course of the study. Although Kehoe did not give the
regression lines of blood lead versus time for each subject, they
can be calculated from the data in his original figure,
reproduced as Figure V-l (12). The source data from Subject s.
W. for the calculation of this line are retabulated in Table v-2.
The slope of the regression line for Subject S. W. while
ingesting a total of 600 ug of lead each day was significantly
different from zero (t=2.82, p less than .01), whereas the slope
was not significantly different from zero during his control
period. The actual regression line as calculated from the data
in Table V-2 and shown in Figure V-2 is as follows:
V-4
-------
y = 36.5 + 0.70 (x - 7.5)
where y = predicted whole blood lead level at time x
and
x = time in 28-day periods
The best fit for these data may be a curvilinear rather than a linear
function, in which case, blood leads would level off about 40 ^ig/100g rather
than continuing to increase indefinitely.
This equation predicts that a blood lead concentration of 40
ug/lOOg would be reached in 12.5 28-day time periods with a 95%
confidence interval ranging from 8.9 to 16.1 time periods. In
other words, a subject ingesting only a 300ug lead supplement to
the 300 ug in his diet would theoretically reach a blood lead
level of 40 ug/lOOg in just less than one year. This prediction
may, of course, be dependent upon the relatively high blood lead
baseline (30-32 pg/lOOg) in subject S.W. when supplemental lead
feedings were initiated and may not accurately reflect any
additional lead intake in subject S.W. due to airborne lead. It
should also be noted that this 600ug figure is consistent with
the World Health Organization's maximum recommended intake of
lead for adults of 50ug of lead/kg/week, the equivalent of SOOug
of lead intake daily for a 70kg man (13).
As described in Section III, urinary delta-aminolevulinic
acid excretion begins to increase as blood lead content rises
above a level of about 40pg/100g. Such an increase in urinary
ALA excretion is generally considered indicative of biochemical
changes in the tissues that are undesirable and physiologically
V-5
-------
significant (14). Based upon Kehoe's data, a daily lead
ingestion of 600ug (with an absorption of 60ug) could cause blood
lead to increase to a level associated with increased urinary ALA
excretion (i.e., 40ug of lead/100g). In this context, one can
estimate the additional daily lead intake in the diet or in the
air necessary to increase lead in blood to this level.
Calculations of this nature are presented in Table V-3. If
average dietary intake is estimated to be 200-300 ug of lead, or
an absorbed amount of 20-30 ug daily, an ordinary man would have
to regularly absorb only an additional 30-40 ug of lead daily to
reach a biologically undesirable blood lead level. Assuming 10%
absorption, he could do this by an additional dietary ingestion
of 300-400 ug daily, or by combinations of dietary ingestion and
inhalation. The main concern here, however, is what air lead
exposure level could also result in an increased absorption of
30-40 jag daily?
The daily amount of lead absorbed from inhaled air is the
product of: the airborne lead concentration; the volume of air
inhaled daily; and the percent of lead reaching the respiratory
tract that is absorbed. The airborne lead concentration varies
from place to place. The volume of air inhaled daily has been
estimated at about 23 cubic meters (m^) for a "standard man"
(weighing 70ky, 20-30 years of age, 175 cm tall, and having a
surface area of 1.8 mc) engaged in light work; about 85% of this
V-6
-------
air being inhaled during waking hours (15). Other estimates have
been lower, in the range 15-20m3 of inhaled air daily. As an
example, the amount of lead absorbed from breathing air
containing 1ug/m 3 of lead assuming 30% absorption and inhalation
of 20m^ of air each day, is 6.0pg. For a constant dietary lead
intake, exposure to increasing airborne lead levels will increase
both the absolute amount of lead absorbed by this route and the
relative proportion of total lead absorption into the blood which
comes from air.
Air levels necessary to increase a man's total daily lead
absorption by 30 and by 40ug are estimated in Table V-4. A range
of values was calculated by using different parameters for daily
air intake and daily lead absorption from the respiratory tract.
These calculations indicate that a daily air lead exposure of
o
5.0ug/m° for a standard man could increase his daily lead
absorption by 30ug. Such Ambient air lead levels attributable
largely to lead in gasoline have been noted in portions of
several U.S. cities at the present time (16).
Experimental data on humans exposed to particulate lead in a
chamber support these theoretical calculations (17, 18). The
chemical composition and size of the lead oxide particles in
these experiments were not identical to those emitted from
automobiles; nevertheless, these differences were sufficiently
V-7
-------
small so that inferences can be made regarding effects of
airborne lead among the general population.
Volunteer subjects in New York State living in a chamber were
o o
exposed to airborne lead levels of 10.9ug/m and 3.2uq/m °for 23
hours a day in two separate experiments. Average blood lead
3
levels among the men exposed to 10.9ug/m of lead daily increased
from about 20 to 37ug/100ml of lead in whole blood after 125 days
(18 weeks); average blood lead levels among a second group of men
exposed to 3.2pg/m^ of air lead for 11 weeks increased from about
19 to 25ug/100 ml of lead in whole blood.
These results are compared to those of Kehoe (12) referred to
earlier in Table V-5. Estimates of the daily total lead
absorption for the study subjects breathing lead at 10.9ug/nr and
Dr. Kehoe's subject S.W. are shown in this table. The results
of both experiments are similar and, while the New York State
subjects might have had a somewhat greater total daily lead
absorption, their average blood lead levels increased from 20-
37ug/100ml in only a little over four months.
The experiment in New York State at lead exposure levels of
3.2ug/m^ also showed that the men who had been previously exposed
to airborne lead at 10.9ug/m , responded differently to their
subsequent re-exposure, compared to subjects not so previously
exposed.(18) The previously exposed men had consistently higher
V-8
-------
3
blood lead levels before and after exposure to 3.2ug/m than the
men without such exposure. This observation is consistent with
Goyer's recent suggestion that repeated exposure to lead may
alter pathways of lead detoxification and excretion (19).
Several epidemiologic studies have investigated the relation-
ship between blood lead levels and airborne lead exposures. A
study, commonly referred to as "The Seven City Lead Study",
showed a positive but not statistically significant correlation
between average blood lead levels and average annual airborne
lead exposures ranging in concentration from 0.17 to 3.39
ug/m^.(20). Exposure was estimated from measurements made at
sampling stations generally located within one mile of the homes
of subjects being studied. Based upon consistent differences
between average blood lead levels in urban and suburban dwellers,
the authors concluded, "It is probable that these observations
partially reflect lead absorption from ambient atmospheres
differing in lead concentration. . . but that factors other than
the atmospheric lead level are of relatively greater importance
in determining the blood lead levels in population groups." This
conclusion was strengthened by further analysis of the study
results (21) which found that air lead was a significant though
not the most influential factor affecting blood lead levels.
A study by Daines et al. obtained more accurate exposure
information by studying the effect of distance of residence from
V-9
-------
highways upon blood lead levels among black females (22) .
Average annual air lead levels on the front porches of homes
located 3.7, 38.1, and 121.9 meters away from a highway were
o
U.60, 2.U1, and 2.24 jag/m ° respectively. There was no
significant difference between the outside air lead
concentrations at 38 and 122 meters, but both were different from
the air lead concentration at 3.7 meters from the highway. This
rapid non-linear decrease in airborne lead with distance from the
source has been observed for mobile as well as stationary lead
sources.Concentrations of lead in dustfall also decrease rapidly
with increasing distance from the source. (23-25) Average
annual air lead levels in the front room of houses at the three
sampling points also reflected this non-linear decrease being
2.30, 1.50, and 1.57 ug/m as the distances increased. Average
blood lead levels in the study subjects were 23.1, 17.U, and 17.6
ug Pb/100 q at 3.7, 38.1, and 121.9 meters respectively. The
average blood lead levels at the two more distant sampling sites
differed significantly from the average at 3.7 meters, but did
net differ significantly from each other.
It is of interest to note that among the homes closest to the
highway (3.7 meters), air lead and blood lead levels were
significantly lower for subjects whose homes were air-conditioned
than for similar subjects in homes without air-conditioning.
Another finding was that significant differences in air lead, but
not in blood lead levels were observed for subjects in homes at
V-10
-------
33.4 and 457 meters from a turnpike (22,26). The average outdoor
air lead levels at 33.4 meters and 457 meters were 1.95 and 1.73
3
ug/m ; blood leads at these sites averaged 15.7 and 16.1 ug/100g
respectively. In this experiment the air lead levels, though
statistically different, would not necessarily be reflected in
higher blood lead levels, as daily respiratory lead absorption
nearer the turnpike would only amount to about 1 ug of lead per
day more than at the distant site.
Azar et al. studied thirty male subjects in each of five
locations in the United States (27). Air lead levels were
measured with personal samplers twenty-four hours a day for two
to four weeks and the combined air lead exposure each day ranged
from 0.81 - 1.10 ug/m 3 for office workers in Starke, Florida, and
Barksdale, Wisconsin, to 3.06 for office workers and 6.10 ug/m
for taxi drivers in Los Angeles, California. The average daily
air lead exposure for a group of Philadelphia taxicab drivers was
2.62 ug/m3.
Biweekly blood samples were obtained during the two taxicab
studies and the Los Angeles office workers study; at Starke and
Barksdale, a single blood specimen for each study subject was
obtained at the beginning and at the end of the study.
Limitations in the study design were summarized by the authors
who wrote, "The use of different occupational groups located in
different cities; studying each group at a different time; the
V-ll
-------
lack of data relative to ingested lead; and the lack of detailed
histories and physical examinations are obvious design
deficiencies in this study." Average blood lead levels ranged
from 13.8 jag/100 g in Barksdale to 2U.6 pg/100 g for the Los
Angeles taxi drivers. Although the relationship was not linear,
average blood lead values were generally positively associated
with increasing airborne lead exposure. The study also found
that 79-90% of the combined total airborne particulate lead
exposure was in the respirable range, which is in agreement with
the results from New York City. (28)
Jones et al. studied blood lead and carboxyhemoglobin levels
among London taxi drivers on both the day and the night shift
(29). Significant differences were found in blood
carboxyhemoglobin, but not in blood lead levels, when comparing
smoking and non-smoking day-shift drivers to similar night-shift
drivers. The authors concluded that the day drivers had a
greater exposure to motor car exhaust than the night shift
drivers because they had significantly higher blood
carboxyhemoglobin levels and therefore "it would seem that little
of the lead found in their blood is attributable to the lead they
inhale whilst driving in London streets." Unfortunately, both
differences in smoking intensity between smoking groups, as well
as actual differences in air and dietary lead exposure could
explain these results and neither was measured. Furthermore,
information was not obtained regarding the exposure of the
V-12
-------
drivers when they were off-duty. Thus the authors' original
conclusions failed to consider at least three pertinent
confounding variables.
Two studies of blood lead levels among non-occupationally
exposed people living in smelter communities provide additional
data which support a relationship between blood lead levels and
exposure to lead in air or dustfall. Average blood lead levels
among 10 year old United States school boys living in smelter and
non-smelter communities reflected environmental exposure
rankings, but no quantitative measurements of lead in air or lead
in dustfall were given. (30) However, the study pointed out that
lead fallout on home grown produce did not explain the observed
differences and concluded that increased lead exposure and
absorption probably occurred by the respiratory as well as the
gastrointestinal route. A study of adults living around a
secondary lead smelter in Finland showed that blood lead levels
were negatively correlated with the log of the distance from the
source in meters (31). This study did publish isopleths of
monthly dustfall lead in relation to the point source, but no air
lead values were given. Nevertheless, both studies indicate a
qualitative relationship between blood lead levels and exposure
to lead in air and in dustfall.
Observed relationships between lead in air and lead in blood
did not always fit a simple straight line in the above cited
V-13
-------
epidemiclogic studies. Using the previously stated assumptions
•3
for a "standard man", a person breathing 1 ug of lead/m of air
would absorb a total of 6 jig daily from his respiratory tract and
•J
a person breathing 3 ug of lead/m° of air would absorb a total of
18 ug daily from his respiratory tract. Ultimately this
difference in absorption would be reflected in different blood
lead levels providing other sources of lead intake were
equivalent.
Assuming 10% lead absorption from the gastrointestinal tract
and a range of normal daily dietary lead intake from 100-500 jug,
total lead absorption from the gastrointestinal tract would range
from 10-50 ug each day. The need to measure dietary lead intake
in studies of air lead effects is important since one would not
be able to distinguish a person (Subject A) breathing 1 ug/m^ of
lead in air and eating 340 ug of lead daily from a person
(Subject JB) breathing 3 ug/m •* of lead in air and eating 220 ug of
lead daily, viz:
V-14
-------
Lead^Intake §ubject_A Subject_B
Absorbed from air 6 ug 18 ug
Absorbed from diet !iL_li2 22_ug
Total Daily Lead
Absorption 40 jag 40 ug
Furthermore, variations among individuals with respect to gastrointestinal
as well as respiratory lead absorption must be considered in evaluating
such data.
Since none of the epidemiologic studies of air lead and blood
lead considered both lead in diet and variability of
gastrointestinal and respiratory absorption among individuals
when evaluating air lead-blood lead relationships, it is
understandable why simple straight line relationships between the
two variables are not consistently found. As exposure to
airborne lead increases, dietary variations would become less
likely to confound true differences in blood lead due to air lead
exposure.
The above calculations were made for a "standard man;"
comparable calculations for women are difficult since respiration
and absorption data for women are less complete than those for
V-15
-------
men. While the total dietary intake and total daily respiration
of women are generally less than those of men, women generally
are smaller with proportionately lower caloric and oxygen
requirements. Thus the relative relationships with respect to
lead absorption from the gastrointestinal and respiratory tracts
should be rather similar to those for men. It is even more
difficult to extrapolate such calculations to children because
they are in a phase of rapid growth and the parameters of
interest change in a non-linear fashion. For example, a one year
old child has only about 1/7 the body weight of an adult, yet has
about 1/3 to 1/4 the total daily air intake (6n? ) and about 40-
60% of an adult's total dietary lead intake (130 jag) (32) . Hence,
a child takes in less lead on a total basis, but proportionately
more lead on a body weight basis than an adult. At present, the
ultimate effect of these differences upon lead intake and
absorption in children when compared to adults is not fully
known.
Lead from automotive exhaust which is deposited in city dust
and dirt also is a potential source of exposure for human beings.
A gram of dust or dirt would be only about 1/4 teaspoon, although
this may vary somewhat depending on its characteristics. Since
these dusts often contain 1000-2000 ug/g of lead or more, the
safe intake level of lead for children would be greatly exceeded
if only a small fraction of a teaspoon of dust were swallowed
daily. (33)
V-16
-------
In summary, lead from automotive exhaust contributes to human
exposure both from the air and from fallout. Blood lead levels
exceeding 40 ug/100 g are considered medically undesirable and
may ultimately be harmful. Blood lead levels depend on daily
dietary intake and absorption of respired lead. For a "standard
man" with average dietary lead intake, exposure to airborne lead
concentrations of 5.0 to 6.7 ug/m^ could cause his blood lead
concentrations to reach UO ug/100 g within a year. Airborne lead
3
levels near to or in excess of 5 ug/m have been observed in
several U. S. cities.
Lead in dust and dirt poses another important source of
exposure, especially for small children. Daily ingestion of
relatively small quantities of dirt or dust (less than 1 gram or
about 1/U of a teaspoonful) containing 1,000-2,OOOppm of lead
would be medically undesirable. Although dustfall exposure to
lead is still often considered an hypothesis, much of the
available evidence is consistent with this hypothesis. Thus,
present day lead exposure to air or dusts in some sections of
large cities leaves little or no margin of safety compared to
those concentrations associated with biomedical harm.
V-17
-------
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TABLE V-l
Amount of Lead Absorbed from Air
in Relation to
Airborne Lead Concentrations
Among Adults
Daily Lead Absorbtion
Lead in ~ Percent
Air (ug/m) From Air+ Total* From Air
0 0 30 0
1 6 36 17
2 12 42 29
3 18 48 38
4 24 ' 54 44
5 30 60 50
3
+Assumes 30% absorption and 20m daily respiration.
*Assumes 10% absorption of a daily dietary intake of 300 yg
of lead.
-------
TABLE V-2
Regression of Average Blood Lead Level
Versus Time in a Subject* Ingesting a Total of
600 ug of Dietary Lead Daily
x. y_ where:
0 32 x = time in 28-day periods
1 30
2 25 y = average whole blood lead level
3 34 for a 28-day period in jjg/100 g
4 33 of blood.
5 37
6 46 y = 36.5 + 0.70 (x - 7.5)
7 33
8 34 Sx = 4.76
9 42 Sy = 5.53
10 39 Sy.x = 4.56
11 40
12 43
13 43
14 38 . .
15 35
*Reference 12. Subject S. W., average blood lead values taken from
Figure 10., Lecture II.
-------
TABLE V-3
Calculated Difference in Daily Lead Intake
Between a Biologically Undesirable Amount and the
Amount in the Normal Adult Diet
Daily Lead Intake
Ingested Absorbed
Biologically Undesirable Amount+ 600 ug 60 ug
Normal Adult Diet 200-300 jjg 20-30 ug
Difference 300-400 ug 30-40 ug
+Continued daily intake of. this amount could cause blood lead
levels to rise to about 40 ug/100 g of whole blood with the consequent
increased excretion of delta-aminolevulinic acid in the urine.
-------
TABLE V-4
Estimated Airborne Lead Exposures Which Could Cause
Adult Male Blood Lead Levels to Reach
40 ug/100 g of Whole Blood
Common Daily
Dietary Lead
Absorption
20 ug
30 ug
Increase Required
to Reach 60 ug Daily*
40 ug
30 ug
Airborne Lead Exposures Which
Would Cause the Designated Increase
Standard(a)
Man
6.7 ug/m^
5.0 ug/mj
Highest(c)
Case
Least(b)
Case
15.7ug/m 5.4
4.0 ug/m
+Experimentally in a human, absorption of 60 ug of lead daily caused his
blood lead levels to reach 40 ug/100 g of whole blood. (12)
(a) Standard Man = 20m
b) Least Case = 15m
c) Highest Case = 20m 3x 37% absorption
30% absorption
x 17% absorption
-------
TABLE V-5
Estimated Daily Total Lead Absorption
in Two Experimental Studies
Exposure
Source
Daily Lead Absorption
New York (17,18) Kehoe's Subject (12)
Chamber Exposure S.W^ Exposure
Diet
10 ug*
30 ug*
Experimentally
Added
U9-60 ug+ (Air)
30 ug* (Diet)
Daily Total
Lead Absorbed
59-70 ug
60 ug
*Assumes 15m3 daily respiration (since the men in both experiments were sedentary)
and 30-37% absorption of 10.9 ug/m3 of lead in air.
*Assumes 10% absorption of dietary intake.
-------
REFERENCES
1. Joint FAO/WHO Expert Committee on Food Additives;
"Evaluation of Certain Food Additives and the
Contaminants Mercury, Lead and Cadmium; WHO Technical
Report Series, No. 505, 1972.
2. Airborne Lead in Perspective, A Report Prepared by the
Committee on Biologic Effects of Atmospheric Pollutants,
National Academy of Sciences, Washington, D. C., 1972
p. 50.
3. Airborne Lead in Perspective, op.cit., pp. 52-53.
4. Thompason, J.A.; Balance Between Intake and Output of
Lead in Normal Individuals. Brit. J. Industr. Med.,
28:189-194, 1971.
5. Alexander, F.W., H.T. Delves, and B.E. Clayton, the
uptake and excretion by children of lead and other
contaminants. Proceedings of An International
Symposium on the Environmental Health Aspects of Lead,
CEC, CID, Luxembourg, May 1973, pp. 319-331.
V-18
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6. Goyer, R.A., and B.C. Rhyne, "Pathological Effects of
Lead," Int'l. Rev. Exp. Path., 1973, 12:pp. 1-77.
Ifcid.
8. Airborne Lead in Perspective, op.cit., pp. 65-67.
9. Cole, J.; International Lead Zinc Research Organization,
New York City; Testimony presented to EPA, Dallas,
Texas, April 28, 1972.
10. Airborne Lead in Perspective, op.cit., pp. 65-67.
11. Rabinowitz, M.A., G.W. Wetherill, and J.D. Kopple,
"Study of lead metabolism using stable isotope
tracers," paper presented at EPA-NIEHS Conference on
Low Level Lead Toxicity, Raleigh, N.C., Oct 1-2, 1973
and M. B. Rabinowitz, G. W. Wetherill and J. D. Kopple,
"Lead Metabolism in the Normal Human: Stable Isotope
Studies," Science 182:725-727, November 1973.
12. Kehoe, R.A.; The Metabolism of Lead in Man in Health
and Disease. The Harben Lectures, 1960. McCorquodale
and Co., Ltd., London, England, 1961. 81 pages.
Reprinted from the J. Roy. Inst. Public Health Hyg.
V-19
-------
24:81-97, 101-120, 129-143, 177-203; 1961.
13. Joint FAO/WHO Expert Committee on Food Additives, op.cit.
14. Airborne Lead in Perspective, op.cit., p. 110.
15. Airborne Lead in Perspective, op.cit., p. 51.
16. Shearer, S.D., EPA; Testimony presented at EPA Public
Hearings on Regulation of Fuels and Fuel Additives, Los
Angeles, California, May 2-4, 1972.
17. Knelson, J.H., R.J. Johnson, F. Coulston, L. Goldberg
and T. Griffin; "Kinetics of Respiratory Lead Intake in
Humans:" Proceedings of the International Symposium on
Environmental Health Aspects of Lead;" CEC, CID, Luxembourg,
May 1973, pp. 391-401.
18. Knelson, J.H., F. Coulston, L. Goldberg and T. Griffin;
The Role of Clinical Research in Establishing standards
for Atmospheric Lead. Presented at the Conference on
Heavy Metals, VDI-Kommission Reinhaltung der Luft,
Dusseldorf, Germany, February 22, 1973.
19. Goyer, R.A.; "Lead and the Kidney" in Current Topics in
Pathology, Springer-Verlag, Berlin, 55:147-176, 1971.
V-20
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20. Tepper, L.B. and L.S. Levin; A survey of Air and
Population Lead Levels in Selected American Communities.
Department of Environmental Health, College of Medicine,
University of Cincinnati, Cincinnati, Ohio. Final
Report (Contract PH-22-68-28), December 1972. 73 pages.
21. Hasselblad, V. and W.C. Nelson; Additional Analyses of
the Seven City Lead Study. Human Studies Laboratory,
National Environmental Research center, U.S. Environmental
Protection Agency, Research Triangle Park, N.C. In-house
Technical Report, March 15, 1973.
22. Daines, R.H., D.W. Smith, A.F. Feliciano and J.R.
Trout; Air Levels of Lead Inside and Outside Homes.
Ind. Med. Journal 41:26-28, October 1972.
23. Airborne Lead in Perspective, op.cit., p. 29.
24. Creason, J.P., O. McNulty, L.T. Heiderscheit, D.H.
Swanson and R.W. Buechley; Roadside Gradients in
Atmospheric Concentrations of Cadmium, Lead and Zinc.
Trace Substances in Environmental Health V. A
Symposium, 1972. pp. 129-142.
25. Helena Valley, Montana, Area Environmental Pollution
V-21
-------
Study, U.S. Environmental Protection Agency, Office of
Air Programs, Pesearch Triangle Park, N.C., January 1972.
GAP No. AP-91, xiv + 179 pages.
26. Trout, J.R.; Statistics Center, Rutgers University, New
Brunswick, N.J. 08903. Personal communication to Dr.
K. Bridbord, U.S. ENvironmental Protection Agency,
March 21, 1973.
27. Azar, A., K. Habibi and R. Snee; Relationship of
Community Levels of Air Lead and Indices of Lead
Absorption; Proceedings of an International Symposium
on Environmental Health Aspects of Lead; CEC, CID,
Luxembourg, May 1973, pp.581-59U.
28. Ferrand, E.F., Assistant Commissioner for Scientific
Affairs, New York City Department of Air Resources, New
York City, New York. Testimony submitted to EPA,
April 11, 1972.
29. Jones, R.D., B.T. Commins and A.A. Cernik; Blood Lead
and Carboxyhemoglobin Levels in London Taxi Drivers.
Lancet, 302-303, August 12, 1972.
30. Hammer, D.I., J.F. Finklea, R.H. Hendricks, T.A.
Hinners and W.B. Riggan; Trace Metals in Human Hair as
V-22
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a Simple Epidemiologic Monitor of Environmental
Exposure. Trace Substances in Environmental Health V.
A Symposium. D.D. Hemphill, Ed. University of Missouri,
Columbia, 1972. pp. 25-38.
31. Nordman, C.H., S. Hernberg, J. Nikkanen and A. Ryhanen;
Blood Lead Levels and Erythrocyte Delta-Aminolevulinic
Acid Dehydratase Activity in People Living Around a
Secondary Lead Smelter. Work - Environm. - Hlth 10:19-
25, 1973.
32. King, E.G.; Maximum Daily Intake of Lead Without Excessive
Body Lead Burden in Children. Amer. J. Dis. Child.
122:337-339, 1971.
33. Ibid.
V-23
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VI. Lead _Exj3Qsure_f r om Dust fall
Recent surveys of urban environments reveal substantial
levels of lead contamination in dust and dirt found in streets as
well as in homes. This contamination represents a potential
source of lead exposure, especially for children. Weathering of
leaded paint from buildings is a major contributor to lead in
dust and dirt (1-U), as is fallout of airborne lead from other
stationary and mobile lead sources. At the moment it is not
possible to give an overall figure quantifying the contribution
that each of these sources makes to lead in dirt and dust. The
discussion to follow summarizes what is known about these
contributions as well as the implications of this contamination.
Lead content of dirt at various distances from houses and
roadways in Detroit was examined by Ter Haar, et.al. (5). Lead
content of dirt two feet from painted frame houses averaged 2,010
ppm lead, while, dirt two feet from brick houses with painted
trim averaged 468 ppm lead. street gutter dirt near these homes
averaged 966 and 1,213 ppm lead, respectively. Lead content of
dirt decreased with increased distances from both roadways and
houses. Lead concentrations in dirt at corresponding distances
from frame houses were similar in city and rural yards. Based
upon these findings, it was concluded by Ter Haar that lead
antiknocks did not contribute significantly to the lead content
-------
of dirt in urban areas. (5) This conclusion, however, does not
adequately reflect the effect of proximity to roadways upon dirt
lead content that was found. Further, these observations were
made in areas with relatively low traffic density and would not
be applicable to all urban situations.
In this context, it has been shown that airborne lead fallout
decreases with increased distances from roadways (6), implicating
lead in gasoline as a contributor to this problem. The effect of
proximity to roadways upon lead levels in soils has previously
been demonstrated (7) . Lead levels in dust samples taken inside
homes located within 5 meters from heavily travelled roadways
averaged nearly 1000 ppm (0.1%) lead, or approximately double the
level in samples from homes located on side streets (8).
Lead concentrations in surface soils of city parks have been
found to range from 194 to 3,357 ppm and lead levels in dust from
residential and commercial sites in midwestern cities averaged,
1,636 and 2,413 ppm, respectively (9). Dust lead levels in
street sweepings from Washington and Boston usually ranged from
0.1 to 0.25% and at times exceeded 0.5% (10,11).
Lead levels in dust inside homes of Boston have ranged from
0.1-0.2% (12) and have exceeded 0.5% in Birmingham, England (13)
Samples of dust from inside elementary school classrooms in
VI-2
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Philadelphia and dirt from playgrounds adjacent to those schools
routinely contained 0.2-0.3X lead, with levels greater than 1%
found at two locations (14). From these studies it is not
possible to determine the relative contribution that erosion of
lead based paint compared to airborne sources made to lead in
housedusts. In some of the measurements in Philadelphia,
contamination by lead fallout from industrial sources was
believed to have occurred.
Concentrations of lead in house dust have been observed to
vary with the amount of lead fallout from the air (15). House
dust lead levels taken from middle income homes in two New York
City communities which were likely free of peeling lead paint
averaged 608.6 ppm and 7m.5 ppm, respectively. These values
were 2-3 times higher than the mean values from homes in a
control community where dustfall lead was about 1/10 - 1/5 as
great. In this study, lead in housedust as well as lead in soil
from each community followed the dustfall gradient implicating
airborne sources largely due to lead in gasoline as important
contributors to this contamination. Erosion of lead based paint
could, of course, also have been a contributing factor. Lead
concentrations in hair among subjects living in these homes
(adults and children combined) were not found to consistently
follow these exposure differences. However, additional analyses
are necessary to determine if lead exposure was different
depending on age within each area and if hair lead levels
VI-3
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reflected exposure differences among the young children in
different areas. It should be noted that hair leads among
children in this study may not strongly reflect housedust lead
exposure differences since opportunities to place dust
contaminated objects into their mouths during unsupervised
activities may be much lower for middle income than for low
income children.
To date, ingestion of lead-contaminated dirt or dust has
rarely been suspected of causing clinical lead poisoning, but
this source of lead generally has not been investigated in cases
of excessive lead exposure. A report from Charleston, South
Carolina has shown that soil from yards of homes where cases of
pediatric lead poisoning occurred contained greater
concentrations of lead than soil in yards of randomly selected
homes (16). The cases of lead poisoning also were most frequent
in areas of the city with high soil lead concentrations. A
quantitative assessment of the sources responsible for high soil
lead concentrations in Charleston is not possible from this
study. In particular, weathering of outdoor paint as well as
ashes, pesticides and automotive exhausts were all believed to
have contributed. This study concluded that "... these facts
further support the theory that children in Charleston can get
lead poisoning by eating dirt."
VI-4
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In contrast to these findings, a study from England has shown
that average blood lead levels in children residing in an area
with soil containing 10,000 ppm lead were only 4 jag/100 ml higher
than in children from a community with soil containing 500 ppm
lead (17). Why children in Charleston, but not in England,
appeared significantly affected by residence in areas with high
soil lead content is not certain. Perhaps this difference was
due to a greater incidence of pica among children in Charleston
or the more frequent presence of additional sources of lead in
Charleston such as leaded paint. Differences in biologic
availability of lead bound to soil in England compared to
Charleston may also be important. Lead in dirt and dust which is
not tightly bound to soil likely has greater biologic
availability than lead which is bound to soil. It should also be
noted that lead in the form of fine dusts may be more readily
absorbed from the gastrointestinal tract than comparable
quantities of lead in paint chips due to the vastly increased
surface area in these fine dusts.
In this context, rats fed lead-contaminated top soil gathered
near a lead smelter in El Paso at a dose of Img lead/day for 28
days, showed blood lead increases of 20 ug/lOOml over controls on
a low lead diet (18). Similar results were seen after feeding
rats lead contaminated dust (1-2% lead) from city highways and
automobile tunnels (18). Lead contaminated dirt (6600 ppm) from
expressways in Chicago has also been noted to increase blood and
VI-5
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soft tissue lead content after being fed to rats (19). These
results suggest that lead in dust, both that gathered near the
lead smelter and that originating from emissions of automobiles
burning lead additives, although of different chemical
composition and perhaps somewhat different particle size, is
comparably absorbed when fed to experimental animals.
In recognition of the possibility that ingestion of lead-
contaminated dirt and dust could contribute to pediatric lead
exposure, the National Academy of Sciences Lead Panel concluded
(20):
"The swallowing of as much as 1g of such dust could result in
the oral intake of an amount of lead that exceeds by a factor
of 10 or more the estimated mean daily intake of lead from
normal food and drink in nonexposed young children ... For
a child with pica for paint, the combination of the ingestion
of a few chips of paint and an increased intake of lead from
contaminated dusts would provide a total lead intake
sufficient to cause symptomatic illness."
There are many factors which place young children potentially
at a greater risk to lead exposure from dust than adults. The
behavioral patterns of children expose them to large amounts of
dust. This was demonstrated in a study from El Paso, Texas (21).
In a neighborhood near a lead smelter, with high concentrations
VI-6
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of lead in air (5ug/m^) and in surface soil (0.1-0.5%) , blood
lead levels of both children and adults were found to be
elevated. Air lead, blood lead and surface soil lead
concentrations all decreased with increased distance from the
smelter implicating this source as the probable causal factor.
Under these circumstances, 80% of the children between 1 and H
years of age had blood lead levels in excess of 40pg/100g, a
frequency much higher than seen among older children and adults.
This suggests a special exposure route for young children, not
only in dry areas where little or no vegetation exists to hold
outdoor dust in place, but also in typical urban situations (25, 38, 43).
Preliminary data suggest that airborne lead concentrations
tend to be greatest at ground level, and to decrease with
increased elevation (8,22). Therefore, young children, with
their shorter height, may be exposed to greater amounts of
airborne lead and lead-contaminated dust than older, taller
individuals. The normal play activities of children can include
placing materials or their hands, contaminated by leaded dusts,
into their mouths (23-25). A moistened lollipop dropped to the
ground can pick up 0.5g of dirt (22), which would contain 2,500ug
of lead if the dirt contained 0.5% lead. This quantity of lead
is an order of magnitude greater than the amount of lead
routinely found in "the daily diet of children.
VI-7
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A Rochester, New York study has demonstrated that lead
contamination on hands of young children living in homes with
high housedust lead levels is significantly greater than on hands
of children living in homes with low house dust lead levels (25).
The lead level in household dust was also significantly elevated
in inner city homes where at least one child with moderately
elevated blood lead resided compared to suburban homes. Since
blood leads were not determined in all subjects, it is not known
with certainty whether more lead on the hands was associated with
increased blood leads in these children. These data are
consistent with the frequent contamination of finger prick blood
lead specimens by lead on hands of children indicating the
widespread occurrence of such contamination.(25)
These data do not firmly establish the sources responsible
for the elevated lead concentrations in urban housedust. Of note
is that pre-1940 homes had greater quantities of lead in
housedust than post-1940 homes (25) . This observation was also
made in Boston(11). Though this difference could in theory be
accounted for by higher concentrations of lead in paint in older
homes, it could also be explained by greater ventilation and
increased lead fallout in older homes especially since newer
homes are more frequently air conditioned (11). Peeling lead
paint was likely not the sole contributor to lead in housedust in
the Rochester homes studied since an association was not found
between the presence of peeling lead based paint in homes and
VI-8
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increased lead in house dust. This in part could have been due
to residual leaded dusts from paint which were ground into the
floor prior to repainting of deteriorating surfaces or from
deterioration of repainted surfaces themselves. With the
available data, one cannot quantitatively assess the relative
contribution of erosion of lead paint and of other lead sources
to the total lead content of house dust. As noted earlier, lead
in housedust is a function of airborne lead fallout and proximity
of homes to roadways.
In separate Rochester surveys (25) average blood leads among
3-4 year old urban children (about 40pg/100g) were approximately
double those among suburban children. Blood leads much above 60
ug/100 g were not common in the urban children, which would be
expected if ingestion of paint flakes containing very high
quantities of lead were the primary mechanism of exposure.
Nearly 50% of these inner city children had blood lead levels
between 40 and 60ug/100g implicating sources of exposure less
massive than that routinely found in chips of paint. There were
no known industrial sources of lead pollution in the inner city
study area and high lead levels in water were also ruled out as
an important factor. To the extent that airborne lead fallout,
in large part due to automobiles, is greater in urban compared to
suburban areas, lead in gasoline would have contributed to lead
in housedust found in these Rochester homes. Traffic density in
this study area was relatively low so the contribution of lead
VI-9
-------
from gasoline was no doubt less than in areas with high traffic
density. These data suggest that ingestion of leaded dusts were
in part responsible for increased lead exposure among Rochester
children. This study does not quantify the contributors to lead
in housedust whether from airborne sources, chalking or peeling
of paint, or perhaps pulverization underfoot of paint chips shed
from the walls.
Lead-210, an isotope usually present at very low levels in
leaded paint and in significantly higher concentrations in
fallout dust was employed to evaluate the relative quantities of
lead containing dust and paint ingested by young children (5).
The hypothesis examined was that if a child with an elevated lead
body burden had high stable lead but normal level-210 in his
feces, then lead elevation was probably the result of paint
ingestion. If high stable lead and high lead-210 were found in
the feces, then this would favor lead in dust and dirt as
contributing to the lead body burden.
Eight children suspected of having elevated lead body burdens
were compared to ten children living in good housing where lead
poisoning was not a problem. Fecal excretion of both stable lead
and lead-210 was determined in both groups of children. The
children suspected of having elevated lead body burdens, with two
exceptions who were normal, had stable lead concentrations in
their feces that were 4 to 400 times higher than found in the
VI-10
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normal children. There was, however, no difference in lead-210
fecal excretion between groups. Based upon these findings, it
was concluded that children suspected of elevated lead body
burdens did not ingest dust.
The effect that lead-210 in the diet or in the air could have
had upon these results was not adequately considered in this
study. Unless lead-210 intake from the diet and the air were
known to be equivalent in each group, no firm conclusions are
warranted regarding non-dietary sources of lead-210.
Unfortunately, no measurements of lead-210 in the diet were made,
which for adults in the United States range from 1-2
picocuries/day (26-28) . Airborne sources which have been
estimated to contribute 8-32% (28) and in one instance nearly 50%
(27) of total daily lead-210 absorption into the blood were also
not measured. From the data presented (5) , one can calculate
that the fecal excretion of lead-210 by these children was
generally less than 1 picocurie/day. Except for one child who
almost certainly had recently ingested paint chips, fecal stable
lead excretion in the group suspected of elevated lead body
burdens averaged only about 300 ug/day or 5 times greater than in
the normal children. This level of lead excretion is far below
the 14,000 ug/day associated with lead poisoning from ingestion
of paint chips (2). Though these findings do not rule out
ingestion of paint as dust or ingestion of paint chips prior to
fecal lead determinations in these children, they also do not
VI-11
-------
rule out ingestion of dirt or dust contaminated by lead sources
other than paint prior to examination.
An additional important observation is evident from this
study. The lead-210 which was used as a tracer is a product of
radon decay in the atmosphere. Lead-210, thus produced, attaches
to air suspended particulates including lead from automobile
exhausts as well as from other sources. The fact that relatively
high concentrations of lead-210 originating in the atmosphere
were found in vacuum cleaner sweepings, in yard dirt and in
street dirt means that atmospheric particulate fallout, known to
routinely contain stable lead, was contaminating these samples to
some degree.
Extensive screening programs in the United States
concentrating on inner city children, have demonstrated that
approximately 25% of these children were significantly exposed to
lead (blood lead levels of UOjag/lOOg or above) (29-31) . Lead-
based paint has long been recognized as the principle source of
lead overexposure among young children. However, it is not clear
that lead-based paint alone accounts for this widespread degree
of exposure.
For example, screening programs have detected high levels of
lead exposure in children residing outside the central city,
where exposure to lead based paint would be expected to be less
VI-12
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than in the central city environment (24,32,33). In a study from
Oregon, 50% of children with elevated blood lead levels were
found to live in housing where lead paint was not considered
accessible to them (34). In New York City, only 50% of children
with blood lead levels between 35 and HUug/ lOOg could be
associated with living in homes containing peeling paint of 1% or
greater lead. Nearly 20% of this group lived in homes in which
no peeling paint was identified (35).
The source of excessive lead exposure is thus not always
directly related to paint in a significant percentage of cases.
This situation may reflect exposure to lead paint in former
homes, or in places other than those inspected. Further, closer
or repeat inspection will often reveal sources of peeling lead
paint in the home which were not initially detected. Additional
sources of lead in food, water, pottery, toys, pencils, solder,
etc., are also possible factors in cases of unidentified routes
of exposure. Lead contaminanted dust and dirt, especially
prevalent in urban areas, may also be an important contributing
factor. Further information is required to arrive at a
definitive assessment of the significance of this source of lead
contamination.
It is clear that peeling lead based paint remains an
exceedingly important problem, and even exists outside of inner
city areas (36). In one New York City study, 100% of apartments
Vl-13
-------
in a high risk lead poisoning neighborhood showed high lead
levels on paint surfaces (37). These studies, and extensive
clinical experience, indicate that leaded paint is primarily
responsible for the great majority of overt clinical lead
poisoning in children, although non-paint lead sources would
decrease the amount of lead from paint required to cause serious
damage. Education and screening programs have been noted to
decrease the reported frequency of clinical lead poisoning in
children (38). Whether or not these screening programs are
sufficient in themselves to adequately reduce the frequency of
undue lead exposure among children is less certain.
For example, in the initial year of the Chicago lead
screening program, 8.5% of children tested had blood leads of 50
ug/100 ml or more (38). In 1968 the fraction of children with
blood leads in this range dropped to 3.8% and in 1969 to 1.5%.
Figures for 1970 and 1971 were 2.1% and 2.3% resoectively.
Hence, despite an initial decline and a continued and vigorous
program to decrease lead paint exposure, the percentage of
children tested with blood leads of 50 ug/100 ml or above has
either remained relatively constant or may have actually
increased slightly in recent years. Statistics for 1972 confirm
this increasing trend and show that U.1% of children screened
that year had blood lead levels of 50 ug/100 ml or above (U2).
Thus, though efforts to reduce lead paint exposure continued, the
reported frequency of undue lead exposure but not severe lead
VI-14
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poisoning appears to be increasing in Chicago. These findings
are unexplained by changes in method of blood lead collection or
analytical techniques because these procedures have not been
altered since the beginning of the Chicago screening program in
1967. This increasing trend is particularly significant since
screening programs initially concentrate in highest risk areas
for lead paint and then at least to some degree gradually expand
to include other areas of lesser risk. These statistics indicate
the continuing need for vigorous action to prevent lead paint
exposure and also suggest that sources of lead other than paint
are having an incremental effect upon lead paint exposure in
Chicago.
There has admittedly been considerable controversy as to
whether or not partial or even total removal of lead from
gasoline would have any impact upon the lead exposure problem in
this country (39,40). In this context, children residing in pre-
World War II housing have been observed to have higher blood lead
levels than children residing in newer housing projects. One
such survey conducted in Washington, B.C. during 1970 indicated
that the lowest blood lead levels among children tested for lead
poisoning were found in areas of the city where public housing
projects had been built since 1942 (43). No child living in a
recently built housing project, where exposure to lead based
paint would be minimum, had a blood lead level above 40 ug/lOOg.
Blood lead determinations in this survey of 808 children showed
VI-15
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that 5.8% of all children tested had a blood lead of at least 40
ug/lOOg and that nearly 10% of children between 1-3 years of age
had blood lead levels in this range. It should be noted that
these results are somewhat lower than those from subsequent
Washington, D.C. surveys in which 22.0 and 39.2% of children
tested were found to have blood lead levels of 40 ug/lOOg or
above (44,45).
This original Washington survey does indicate that the
frequency of lead poisoning and undue lead absorption in children
would be greatly reduced if lead paint were nearly eliminated.
These findings however, do not rule out an important contributing
role for sources of lead other than paint among children residing
in home environments where lead paint is present.
For example, location of residences near urban roadways and
in areas of high traffic density has been shown to significantly
affect the degree of undue lead absorption among children also
exposed to paint (46). In this study, the effect of residential
location upon blood lead was examined retrospectively among over
5,000 children tested for lead poisoning in Newark, New Jersey
during 1971. Among those children residing within 100 feet of a
major roadway, 49.3% were found to have blood lead levels between
40-59 ug/100 ml and 8.1% had blood lead levels of 60 jig/100 ml
and above. Children residing 100-200 feet and greater than 200
feet from major roadways were not significantly different from
VI-16
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each other. Approximately 25% of blood leads in both groups were
between 40-59 ug/100 ml and 3-5% were at least as high as 60
ug/100 ml. When these groups, however, were compared to children
residing within 100 feet of major traffic arterials a marked
difference was observed with twice the frequency of undue lead
absorption found in children living nearest the roadway.
In children residing within 200 feet of a major traffic
artery the extent of undue lead absorption was observed to
increase when average weekday traffic densities exceeded 24,000
vehicles per day. In such instances 51.3% of children had blood
leads between 40-59 ug/100 ml and 10.8% of children had blood
leads of 60 ug/100 ml or above. Comparable rates for children
residing in areas with weekday traffic densities below 24,000
vehicles per day were 36.6% with blood leads between 40-59 ug/100
ml and 5.1% with blood leads of at least 60 ug/100 ml.
These results could conceivably be confounded by existence of
poorer quality housing nearest roadways and by racial and social
class differences among residents near major roadways. However,
the fact that no difference was noted in blood leads among
children residing within 100-200 feet of roadways compared to
children residing beyond 200 feet suggests that these other
factors were likely not major confounding variables.
VI-17
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Earlier studies in Newark found positive and statistically
significant,but not overwhelming correlations*between elevated
blood leads and indices of housing status as reflected by number
of housing units built prior to 1950 and the number of housing
units considered deteriorated and dilapidated in the census
tract. (47) correlation coefficients for these indices and 'rates
of excessive lead absorption (blood lead of 60 ug/lOOg and above)
and elevated blood lead (40 pg/lOOg and above) ranged from 0.35
to 0.49. The relatively low correlations which were observed
suggests that factors other than housing status also were
important. For example, in seven census tracts with low
potential hazard scores based on housing status, high rates of
excessive lead absorption were observed.
Findings such as these from Newark indicate that factors
other than housing are important in lead poisoning and that
automotive lead emissions can contribute significantly to undue
lead absorption in children. Because immediate removal of old
lead paint from all existing structures cannot practically be
accomplished,reduction of other sources of lead exposure is
important. If the results from Newark, New Jersey are in any way
applicable to other urban situations, this would indicate that
automotive lead emissions do have a significant incremental
impact upon the lead exposure problem in this country.
VI-18
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In a study in Philadelphia, referred to earlier (14) , 8.4% of
white first grade children who lived and attended private school
in proximity to a major industrial lead source were found to have
dentine lead levels in excess of 300 ug/g, a level associated
with frank lead poisoning. These children resided in older
housing that was generally in good repair but were exposed to
levels of lead in environmental dusts commonly in the range of
3,000-8,000 ppm. The community in which these children lived was
also heavily exposed to automotive lead emissions. In contrast
to these children, 19% of black students attending public school
in the same district but who lived in deteriorating housing had
dentine lead levels in excess of 300 ug/g. When both groups of
children were compared to public and private school children
living in a community free of industrial lead sources and
residing in housing built since World War II striking differences
in dentine lead levels were noted. Only 3% of the public and
6.6% of the private school students in the low exposure community
had dentine lead concentrations in excess of 100 ug/g, whereas
66% of the black public school students and 43% of the white
private school students in the high exposure area had dentine
lead levels greater than 100 ug/g.
Interior dust samples from the public and private schools in
the low exposure community contained an average of 614 ppm lead
(range 293-939 ppm) compared to interior dust samples from
schools in the high exposure community which contained an average
VI-19
-------
of 3,867 ppm lead (range 929-15,680 ppm) . Samples of gutter dirt
in the low exposure community contained an average of 1,507 ppm
lead (range 270-2,626 ppm) compared to an average of 3,262 ppm
lead (range 280-8,201 ppm) for gutter dirt samples in the high
exposure community. These data from Philadelphia are suggestive
that airborne and dust lead largely from industrial sources can
contribute to undue lead absorption in typical urban areas either
by themselves or when combined with paint from deteriorating
housing.
Studies from Philadelphia, Chicago and Newark discussed above
provide persuasive evidence to strongly suggest that sources of
lead other than paint, including that resulting from the presence
of lead in gasoline, play an important role in childhood lead
exposure. These other sources may be especially significant at
levels of exposure below overt clinical poisoning.
The National Academy of Sciences summarized available
information on the ingestion of lead by children in the following
paragraph from its (1972) report
"The extent to which airborne lead in congested urban areas
contributes to increased lead absorption and lead poisoning
in children is not clearly defined. With respect to young
children, it is not a matter exclusively of inhalation and
particle size, inasmuch as young children mouth and actually
VI-20
-------
eat things that are not food rather indiscriminately.
Airborne lead wastes from such sources as automotive
emissions and the weathering and demolition of old buildings
can be expected to have a significant additive effect on the
total intake. This would be sufficient to evoke compensatory
metabolic responses that are now considered subclinical (such
as increased urinary ALA), at the very least. It may be
estimated that dustfall from airborne lead, if swallowed, can
make a significant contribution to a small child's total lead
intake and thereby contribute to the occurrence of lead
poisoning, especially in urban areas. Even so, the direct
ingestion of lead-pigment paints is clearly the principal
environmental source in cases of severe acute lead poisoning
in young children."
In conclusion, clinical experience indicates that leaded
paint is primarily responsible for the great majority of overt
clinical lead toxicity in children. There is, however,
sufficient data to strongly suggest that sources of lead other
than paint play an important role in childhood lead exposure.
These other sources may be especially significant at levels of
exposure below overt clinical poisoning.
Lead in the air, and particularly lead in dust are ubiquitous
sources of lead which may well be important contributing factors
to the problem. Exposure to dirt and dust sufficiently
VI-21
-------
contaminated by lead could reduce significantly the quantity of
additional lead exposure required to produce clinical poisoning
in a child with other sources of exposure. Though exposure to lead
contaminated dirt and dust from automobile exhaust, alone, has
not been shown to be responsible for cases of overt lead
poisoning§ automotive lead has been related to undue lead
absorption in children. At this time, it would be prudent to
decrease the potential air and dust lead exposure. It should be
recognized that further studies are necessary to better
quantitate the sources of lead contamination in dust and dirt and
the magnitude of the contribution that leaded dust and dirt make
to both subclinical and clinical lead overexposure.
VI-22
-------
REFERENCES
1. Hardy, H., et al., "Lead as an Environmental
Poison," Clinical Pharm. and Ther., 12:982-1002,
November 1971
2. Comments submitted by Ethyl Corporation to the
Environmental Protection Agency, March 9f 1973.
pp. V-m - V-19
3. Ce Treville, T.P., "Natural Occurrence of Lead,"
Arch. Env. Health, 8:212-221, February 196U
U. Bertinuson, J.K. and Clark, C.S., "The contribution of
Lead Content of Soils from Urban Housing," Interface,
6: p. 1073, 1973
5. Ter Haar, G. and R. Aronow, "New Information on Lead in Dirt
and Dust as Related to the Childhood Lead Problem," paper
presented at EPA-NIEHS Conference on Low Level Lead
Toxicity, Raleigh, N.C., Oct 1-2, 1973
6. Creason, J.P., 0. McNutty, L.T. Heiderscheit, D.H.
Swanson, and R.W. Buechley; "Roadside Gradients in
VI-23
-------
Atmospheric Concentrations of Cadmium, Lead
and Zinc,11 Trace Substances in Environmental Health V.
A Symposium, 1972 pp. 129-142
7. Airborne Lead in Perspective, A report prepared by
the Committee on Biologic Effects of Atmospheric
Pollutants, National Research Council, National
Academy of Sciences, Washington, D.C. 1972, p.29
8. Darrov*, D.K. and Schroeder, H.A., "Childhood
Exposure to Enviromental Lead," paper presented
before the American Chemical Society, Chicago,
111., Aug. 29, 1973
9. Airborne Lead in Perspective, op. cit., p. 30
10. Fritsch, A. and M. Prival, center for Science
in the Public Interest, Washington, D.C., testimony
submitted to EPA, 1972
11. Krueger, H. Krueger Enterprises, Cambridge, Massachusetts,
testimony submitted to EPA, July 10, 1972
12. Krueger, H. Op. cit.
VI-24
-------
13. Personal communication to L. Lombardo, Public
Interest Campaign, from R. Stephens and A. Townshend,
University of Birmingham, Department of Chemistry,
Birmingham, England, January 8, 1973
14. Personal communication from Dr. I. M. Shapiro, U. of
Penn. School of Dental Medicine, Philadelphia, Penn.
to Dr. K. Bridbord, EPA, July 26, 1973 and H. L. Needleman
and I. M. Shapiro, "Dentine Lead Levels in Asymptomatic
Philadelphia School Children: Subclinical Exposure in High
and Low Risk Groups," paper presented at EPA-NIEHS Conference
on Low Level Lead Toxicity, Raleigh, North Carolina, October 1-2,
1973.
15. Pinkerton, C., J. P. Creason, D. I. Hammer and
A. V. Colucci," Multi-Media Indices of Environmental
Trace Metal Exposure in Humans," presented at 2nd
International Symposium on Trace Element Metabolism
in Animals, June, 1973, Madison, Wisconsin
16. Fairey, F. S., and J. W. Gray, "Soil Lead and Pediatric
Lead Poisoning in Charleston, S.C.", J. South Carolina
Med. Assoc., 66:79-82, March 1970
17. Barltrop, D., and Strehlow, C.D., "The Significance of High
Soil Lead Concentrations in Childhood Lead Burdens,"
VI-25
-------
paper presented at EPA-NIEHS conference on Low Level Lead
Toxicity, Raleigh, N.C., Oct 1-2, 1973
18. "Environmental Lead: comparison of Blood and Tissue Levels
Following Oral Exposure in Rats," EPA Internal Report, ETRL,
NERC-Cincinnati, February, 1973
19. Calandra, J.C., Industrial Bio-Test laboratory, Northbrook
111., Industrial Bio-Test Research Report IBT No. E1733C,
January 10, 1973
20. Airborne Lead in Perspective, op. cit. p. 139
21. Data compiled by Center for Disease Control, HEW, Atlanta,
on human and environmental lead pollution in El Paso, Texas,
1972
22. Personal communication from Dan K. Darrow, Dartmouth
Medical School, Trace Element Laboratory, Brattleboro,
Vt. to R. K. Bridbord, EPA, Washington, D.C.,
February 20, 1973
23. Barltrop, D., "Children and Environmental Lead,"
paper presented at a conference on "Lead in the
Environment," Zoological Society of London, January
27, 1972
VI-26
-------
24. Lin-Fu, J. S., "Preventing Lead Poisoning in Children,"
Children Today, Vol. 2, p2, January 1973
25. Sayre, J.W., Vostal, J., Pless, I.E., and E. Charney,
House and Handdust as a Potential Source of Childhood
Lead Exposure, Am. J. Dis Child, in press, 1973
and Vostal, J., J.W. Sayre, E. Taves and E. Charney,
"Lead Containing House Dust: another Source of Increased
Lead Exposure in Inner City Children," paper presented at
EPA-NIEHS Conference on Low Level Lead Toxicity, Raleigh, North
Carolina, October 1-2, 1973
26. Holtzman, R.B., "Measurement of the Natural Contents of
RaD (Pb-210) and RaF (Po-210) in Human Bone-Estimates
of Whole-Body Burdens", Health Physics 9:pp 385-400, 1963
27. Morse, R.S. and Welford G.A., "Dietary Intake of 210-Pb,"
Health Physics, 21:pp. 53-55, 1971
28. Magno, P.J., Groulx, P.R. and Apidianakis, J.C., "Lead 210
in Air and Total Diets in the United States During 1966,"
Health Physics, 18: pp. 383-388, 1970.
29. Lin-Fu, J.S., "Undue Absorption of Lead Among
Children—A New Look at an Old Problem," New Eng. J.
VI-27
-------
of Med., Vol. 286, pp. 702-710, 1972
30. Fine, P.R., G.W. Thomas, R.H. Suhs, R.E. Cohnberg and
B.A. Flashner, "Pediatric Blood Lead Levels, A Study
in 14 Illinois Cities of Intermediate Population,"
JAMA: 221, p. 1475-1479, September 1972
31. Gilsinn, J.F., "Estimates of the Nature and Extent
of Lead Paint Poisoning in the United States,"
NBS Technical Note 746, December 1972
32. Lin-Fu, J.S., "Vulnerability of Children to Lead
Exposure 8 Toxicity," New England Journal of
Medicine, In Press
33. Personal communication from W. J. Sobolesky, City of
Philadelphia Department of Public Health to K. Bridbord, j
EPA, dated August 6, 1973
34. Personal communication from M. Deas, Department of
Human Services, Multnomah County, Oregon, to K.
Bridbord, EPA, dated March 6 , 1973
35. New York City Bureau of Lead Poisoning Control, data submittec
to EPA, August 31, 1972 and September 12, 1972
VI-28
-------
36. Personal Communication from W. R. Smith, Baltimore
City Health Department, Baltimore, Md., to M. Kanarek,
EPA, Washington, B.C.
37. Lauer, G.R., R.E. Albert, T.J. Knelp, B. Pasternak, C. Strehlow,
N. Nelson and F.S. Kent, "The Distribution of Lead Paint in
New York City Tenement Buildings," Amer. J. Pub. Health,
63: 163-168, February 1973
38. Sachs, H.K., "Effects of a screening Program on Changing
Patterns of Lead Poisoning," Paper presented at EPA-NIEHS
Conference on Low Level Lead Toxicity, Raleigh, North
Carolina, October 1-2, 1973.
39. Personal communication from J. J. Chisolm, John Hopkins
Univ. School of Medicine, Baltimore, Md. to Asst. Administrator
for Air and Water Programs, EPA, Washington, D.C., dated March 6, 1973
40. Personal communications from H. Sachs, formerly Director,
Chicago Lead Poisoning Program to Administrator, EPA,
dated March 5, 1973 and June 15, 1973
41. "Airborne Lead in Perspective," op. cit., p. 140
VI-29
-------
42. Personal communication from H. L. Slutsky,
Coordinator, Chicago Lead Poisoning Program to
J. S. Lin-Fu, HEW, August 28, 1973.
43. Conn, R. H. and D. Anderson, "D. C. Mounts Unfunded
Program of Screening for Lead Poisoning," HSMHA
Health Reports, 86:409-413, May 1971.
44. Lin-Fu, J. S., Undue Absorption of Lead among
Children. A New Look at an Old Problem, New Eng.
J. Med., 286:702-710, 1972.
45. Gilsinn, J.F., Estimates of the Nature and Extent
of Lead Paint Poisoning in the United States,
National Bureau of Standards Technical Note 746,
December 1972.
46. Margulis, H. L., R. J. Caprio and M. K. Joselwo,
Residential Location Ambient Air Lead Pollution
and Childhood Lead Poisoning, Arch. Env. Health,
in Press.
47. Margulis, H. L., R. J. Caprio, A. Stefaniwsky,
and M. K. Joselow, "Surveillance of Lead Poisoning
in Newark, New Jersey—An Ecological Approach,"
VI-30
-------
Rutgers University and the New Jersey College of
Medicine and Dentistry, Newark, New Jersey.
Prepublication draft.
VI-31
-------
VII . Extgnt_gf _Lead
In section IV, it was stated that determination of lead in
blood is at present the best index for evaluating lead body
burden and exposure. However due to limitations of the studies
on blood lead levels in population groups in this and other
countries, it is not possible to make precise estimates of the
number of persons having blood lead levels within a given range.
Problems still exist in the chemical analysis of blood for lead
content. The results of quality control studies from
laboratories in both the United States and Europe show that
sometimes there is a large variation in results among different
laboratories (1) . Reproducible results even within the same
laboratory are not always obtained, as shown in the Seven Cities
Study (2) . It is difficult to accurately estimate the relative
contributions of air and food sources to such blood lead levels
as are found. That air lead makes some contribution is apparent
from occupational data and from experimental exposures. The
limited survey data available make it clear that most of the
adult U.S. population has blood lead levels in the range of 10-30
ug/100 g.
Available information on the extent of elevated blood lead
levels found in this country is presented in Tables VII- 1 & 2.
It can be seen that a small but generally consistent proportion
of the general population has elevated blood lead levels. It is
also evident that a number of specific groups in the population
frequently or characteristically have blood lead levels
-------
distinctly higher than those usually found. Many of these groups
are occupationally exposed to automobile exhaust. Individuals so
exposed in an outdoor environment, such as traffic police,
parking lot attendants, and service station attendants frequently
show elevated mean blood levels with ranges of 20-50ug/100g or
higher (3,4,6-9). The few data on commercial drivers (4,6,7) also
show elevations compared to the general population. Likewise,
the available information on groups exposed to automotive exhaust
in closed environments show consistently elevated blood leads
(4,8,9) (See Table VII-1). These include workers in parking
structures, traffic tunnels, and service and repair garages.
Repairmen and mechanics may, of course, also be exposed to lead
dust and fumes originating from maintenance activities (9).
Blood lead levels found in urban areas are also somewhat
higher than in suburban and rural areas (2-4) (See Table VII-2) .
The source of most lead for the general population is food,
although air is a significant source of lead in urban areas. It
is known that air lead exposures are higher in urban than in
suburban and rural areas. There are no data available to
determine whether or not this is also true for food. The extent
of the contribution, by occupational and avocational lead
exposure, to the lead burden of the general population and to
urban-rural gradients is likewise not well documented.
In recent years it has been found that large numbers of
central city children are overexposed to lead. Surveys have been
carried out in urban areas to search for childhood lead
VII-2
-------
poisoning, which usually results from the ingest ion of chips of
\
peeling lead paint. Other evidence of overexposure was also
found. In nearly all of these surveys, it has been demonstrated
that approximately 25% of the young children tested have blood
lead levels of 40 ug/lOOg or above (most below 50 ,ug/100g) (10-
13) (Table VII-3), which is medically undesirable. The reasons
for this frequency of elevated blood leads are not completely
understood at present. The shapes of the blood lead frequency
distributions suggest that lead sources more homogeneously
distributed than peeling paint and containing less lead than
routinely found in paint chips are making a major contribution.
The rationale for considering lead dusts which originate from
automotive exhaust as a contributing factor was discussed in the
previous sections.
In summary, it is clear that levels of lead in the blood,
indicating elevated exposure, exist to a small but significant
extent in the general adult population, and to a very great
extent among children. There are also a number of large groups
of the population in which undesirable elevated blood lead levels
are commonly found directly related to exposure to automobile
exhausts. Thus much of the excess exposure to lead in the
general population is due at least in part to lead from
automotive exhaust.
VII-3
-------
TABLE VII-1
Extent of Abnormally Elevated Blood Leads
Among Urban Adults
City Exposure Category
Cincinnati Post Office Employees (4)
Firemen (4)
Service Station Attendants
Police (4)
Drivers of Cars(4)
Parking Attendants (4)
Garage Mechanics (4)
(4)
Number
Studied
140
191
130
40
59
48
152
% of Blood Leads
Equal to or Greater
than 40 ug/100 g
2.9
3.0
12.3
12.5
15.0
44.0
67.0
Los Angeles
Area
L.A. Police (4) 155
Pasadena Male City Employees (4) 88
L.A. Female Aircraft Employees (4) 87
L.A. Male Aircraft Employees (4) 291
0.6
3.3
3.3
5.2
Philadelphia
Male Commuters (1)
Police (4)
Downtown Male Residents
(4)
43
113
66
2.3
3.5
4.5
Camden,
New Jersey
Composite
Urban
Samples
Composite
Urban
Samples
Women Living Near Freeways (5) 55
Females from New York, Philadelphia, 423
and Chicago (3)
Males and Females from 6 Cities (3) 833
Taxi Drivers and Office Workers 149
from L.A.; Philadelphia; Barksdale,
Wisconsin, and Starke, Florida (6)
1.8
0.7
2.7*
0
*0nly those above 40 ug/100 g blood lead.
-------
TABLE VII-2
Urban-Suburban Blood Lead Comparisons
In Adults
% Blood Leads Equal to or
Group Studied Number Studied Greater than 40 ug/100 g
Urban Females (2) 423 0.7
Suburban Females 556 0
Phiadelphia Males (4)
Urban 66 4.5
Suburban 23 0
Composite (3)
Urban 833 2.7*
Suburban 162 0
*0nly those above 40 ug/lOOg.
-------
TABLE VII-3
Percentages of Children with Abnormally Elevated Blood Leads
City
Baltimore (10)
Chicago (10)
New Haven (10)
Newark (10)
New York (10)
New York (11)
Philadelphia (10)
Washington (10)
Many Cities (12)
Aurora, 111. (13,14)
Springfield, 111. (13,14)
Peoria, 111. (13,14)
E. St. Louis, 111. (13,14)
Decatur, 111. (13,14)
Joliet, 111. (13,14)
Rock Island, 111. (13,14)
E. Moline, 111. (13,14)
Robbins, 111. (13,14)
Harvey, 111. (13,14)
Carbondale, 111. (13,14)
Norfolk, Va. (13)
New Haven, Conn. (13)
Washington, D. C. (13)
Rockford, 111. (13,14)
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
Number
Tested
655
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
% Blood Leads Equal to or
Greater than 40 jjg/100 g
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
30
31
24
12
24
21
11
12.6
16.4
17.0
22
23
39
.3
.1
.3
.7
.2
.3
.1
.4
.7
.7
.2
19.5
-------
REFERENCES
1. Subclinical Lead Poisoning; Editorial; Lancet; 1:87, January 1973
2. Tapper, L. and L.S. Levin, "A Survey of Air and Population Lead Levels
in Selected American Communities"; Department of Environmental Health
College of Medicine, Univ. of Cincinnati, Cincinnati, Ohio; Final
report (Contract PH-22-68-28), Dec., 1972, Cincinnati, Ohio
3. Hofreuter, D.H.; et.al.; "The Public Health Significance of
Atmospheric Lead", Arch. Env. Hlth. 3:82:88, Nov. 1961
4. "Survey of Lead in the Atmosphere of Three Urban Communities",
Public Health Service. Publ. No.999-AP-12, 1965
5. Daines, R.H. et. al.; "Air Levels of Lead Inside and Outside
Homes"; Indust. Med. 41: 26-28, Oct. 1972.
6. Azar, A., et. al. - Relationship of Community Levels of
Air Lead and Indices of Lead Absorption. - pp 581-594 In:
Proceedings of International Symposium on Environmental
Health Aspects of Lead, Amsterdam, October 2-6, 1972
VII-4
-------
7. Jones, R.D. et.al. - Blood Lead and Carboxyhemoglobin Levels
in London Taxi Drivers - Lancet 2: 302-303, 12 Aug., 1972.
8. Bericht der Eidg. Bleibenzin-Kommission an den Bundesrat uber
ihre tatigkeit im zeitraum 1947-1960. Mitt. Gebiete Lebensmitt.
Hyg. (Bern). 52(3): 135-244, 1961.
9. Tola, S. et. al. - Occupational Lead Exposure in Finland. II. Service
Stations and Garages. - Work Environ. Hlth. 9:102-105, 1972.
10. Lin-Fu, Jane S. - Undue Absorption of Lead Among Children.
A New Look at an Old Problem - New Eng. J of Med., 286: 702-710, 1972
11. Guinee, Vicent F. - Lead Poisoning - Amer. Jour. Med.; 52:283-288,
12. Challop, R.S., and McCabe, E.B.; "Childhood Lead Poisoning: A
Thirty City Neighborhood Survey"; BCEM, USDHEW, May 23, 1972.
13. Gilsinn, J.F., Estimates of the Nature and Extent of
Lead Paint Poisoning in the United States, NBS Technical
Note 746, December 1972
14. Fine, P.R., et.al. Pediatric Blood Lead Levels. "A Study in
14 Illinois Cities of Intermediate Population," JAMA 221:
p. 1479, September 1972.
VII-5
-------
VIII. Summary and Conclusions
Summary
Lead occurs widely in the environment. Its present
distribution is the result of natural occurrence, greatly
influenced by man's activities. In 1971, in the United States,
1,431,511 tons of lead were consumed with over one million tons
used as metallic lead or lead alloys and in storage batteries.
About 135,000 tons were used in coatings and pigments. Of the
264,000 tons used in gasoline additives, more than two-thirds
enters the environment. Combustion of gasoline contributes by
far the largest fraction of lead reaching the environment. Other
sources of lead in the environment are wear and erosion of lead-
containing painted surfaces, and incineration of lead-containing
substances.
Man takes in lead from many sources: water; food; air; and,
particularly in the case of children, from ingestion of lead-
containing non-food items such as paint and dust. It is probable
that lead in dust and dirt is inadvertently ingested by both
children and adults. It is generally agreed that food is the
major source of lead for the general population. A World Health
Organization expert committee reports that according to the
results of total diet studies in industrialized countries, the
total intake of lead from food generally ranges from 200-300 ug
per person per day. WHO further states that based upon available
-------
datar these levels are similar to those found in the past 30-UO
years and that no upward trend in lead levels in food is evident.
Reducing the amount of airborne lead in the environment
constitutes an accessible means for reducing potential human
exposure to environmental lead particularly when that fraction is
large compared with that absorbed from the diet. (Section II)
Lead has not been shown to be biologically essential or
beneficial to man. In sufficiently high quantities, it is
clearly toxic, and, at somewhat lower levels, has been shown to
cause biochemical changes. Lead is also suspected of producing
subclinical neurologic damage.
The studies reviewed in Section III permit no unequivocal
conclusions to be drawn. On balance, they suggest that
subclinical changes are associated with blood lead levels of
approximately 40 ug/lOOg and above. As blood lead levels
increase above 40 ug/lOOg, the likelihood that these changes will
occur increases markedly. Based upon evidence from these
studies, it would seem prudent to regard blood lead levels over
40 ug/lOOg as indicators of lead intake that should be prevented.
The 40 ug/lOOg figure, however, does not represent a sharp
demarcation between health and disease.
Blood lead levels, under most circumstances, serve as a
reasonably accurate measure of lead body burden and have been
widely employed in public health surveillance. It is not
VIII-2
-------
possible at this time to firmly establish a single acceptable
blood lead level protective of all high risk population groups.
It would appear prudent, however, to recommend that the current
U.S. Public Health Service Guideline for older children and
adults, i.e., 40 ug/lOOml whole blood be regarded as a strict
upper limit for younger children. Whether the acceptable upper
limits should be lower than 40 ug/lOOml for the fetus, neonate,
and the woman of child bearing age will require further
investigation. (Section IV)
In Section V, it is shown that lead from automotive exhaust
contributes to increased exposure for humans both from the air
and from fallout. Blood lead levels exceeding 40 ug/lOOg are
considered medically undesirable and may ultimately be harmful.
Blood lead levels depend on daily dietary intake and adsorption
of respired lead. For a "standard man" with average dietary lead
intake, exposure to average airborne lead concentrations of 5.0
to 6.7 ug/m^ could cause his blood lead concentrations to reach
40 jag/lOOg within a year. Airborne lead levels near to or in
excess of 5 ug/m^ have been observed in several U.S. cities.
Lead in dust and dirt is an important potential source of
exposure, especially for young children. Daily ingestion of
relatively small quantities of dirt or dust (less than 1 gram or
about 1/4 of a teaspoonful) containing 1000-2000ppm of lead would
be medically undesirable. Although dustfall exposure to lead is
still often considered an hypothesis, much of the available
evidence is consistent with this hypothesis. Present day lead
VIII-3
-------
exposure via air or dusts in some sections of large cities leaves
little or no margin of safety in relation to those concentrations
associated with biomedical harm.
In Section VI, it was shown that lead emissions from
automobiles contribute to lead present in urban soils, in street
dirt and in house dust. Lead content of soil has been
demonstrated to decrease with increased distances from both
painted houses and roadways. Lead concentrations in fallout dust
from the air also decrease away from roadways. Dust lead levels
in street sweepings from large cities usually range from 0.1 to
0.25% and at times exceed 0.5%. Housedust from urban areas
commonly contains 0.1% lead or higher. Concentrations of lead in
housedust vary with lead fallout from the air and are reported to
be higher in homes located near heavily travelled roadways than
in homes on side streets. Quantities of lead in housedust do not
vary directly with the presence of peeling paint in the home but
they are higher in older homes, reflecting greater amounts of
lead paint, as well as increased atmospheric ventilation and dust
fallout in older homes. Erosion of paint is clearly a
contributor to lead in housedust. Urban dust and dirt, if
sufficiently contaminated with lead represent a hazard to
children, if ingested, with the available data one cannot
quantitatively assess the relative contribution of erosion of
lead paint and of other lead sources to the total lead content of
soil, street dirt and housedust. Nevertheless, it is evident
that lead emissions from automobiles are major contributors to
this contamination.
VIII-4
-------
Clinical experience indicates that leaded paint is primarily
responsible fcr the great majority of overt clinical lead
poisoning in children. There is, however, sufficient data to
strongly suggest that sources of lead other than paint play an
important role in childhood lead exposure. These other sources
may be especially significant at levels of exposure below overt
clinical poisoning.
Lead in air, and particularly lead in dust are ubiquitous
sources of lead, which may well be important contributing factors
in the childhood lead problem. Exposure to dirt and dust, if
sufficiently contaminated by lead, could significantly reduce the
quantity of additional lead required to produce clinical
poisoning in a child with other sources of exposure. Although
exposure to lead contaminated dirt and dust from automotive
exhausts has not been shown to be responsible for cases of overt
lead poisoning, automotive lead has been related to undue lead
absorption in children. At this time, it would be prudent to
decrease the potential air and dust lead exposure. It should be
recognized that further studies are necessary to better
quantitate the sources of lead contamination in dust and dirt as
well as the magnitude of the contribution that leaded dust and
dirt make to both subclinical and clinical lead overexposure.
It is clear that undesirable levels of lead in the blood,
indicating elevated exposure, and elevated lead body burdens
exist to a great extent among children, and to a small, but
significant extent among adults. There are also a number of
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adult groups in which undesirable elevated blood lead levels are
found directly related to exposure to automobile exhausts. Thus,
much of the excess exposure to lead in the general population is
due at least in part to lead from automotive exhaust. (Section
VII)
Conclusions
A small but significant fraction of the adult population has
blood lead levels of 40ug/100g or higher, and such levels occur
in a much larger proportion of urban children. Such levels are
medically undesirable and should be reduced if possible.
Sources of exposure to lead include food, water, air, and
ingested non-food items such as lead based paint and dust.
Food is the largest contributor of lead to the general population.
Lead based paint is the major cause of overt clinical lead
poisoning in children, though sources of lead other than paint
play an important role in childhood lead exposure particularly at
levels below overt poisoning.
Lead in dust and dirt is believed by EPA to contribute to
increased lead levels in man, both through inhalation of
resuspended dusts and at least in children, through inadvertent
U.S. Environmental Protection Agency
VIII-6 Region 5, Library (PL-12J)
77 West Jackson Boulevard, 12th Floor
Chicago, 1L 60604-3590
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ingestion of dirt and dust. This source could significantly
reduce the quantity of additional lead required to produce
clinical poisoning in a child with other sources of exposure.
Automotive lead is a major contributor to lead in dust and dirt
and has been related to undue lead absorption in children.
Lead from all these sources should be reduced to the degree
possible.
Actions have already been taken by the Federal and other
levels of government to reduce the lead content of paint and
further actions in this regard are being contemplated so that
this source of lead will decline with time as older buildings
with leaded paint are replaced. Action has also been taken to
substantially reduce controllable sources of lead in food, and
efforts to further reduce lead in food are continuing. One
controllable source of lead in food is residue from use of lead
compounds as insecticides. Tolerances for these residues are
being reevaluated at this time. Lead in a few drinking water
supplies is higher than desirable, and efforts should be
continued to reduce this source of lead exposure.
In EPA's opinion, lead in gasoline is the most important
remaining source of controllable lead entering the environment.
Reduction of lead in gasoline has shown to reduce lead in the
ambient air. Leaded gasoline results in direct exposure to the
population through inspired air and by presence of lead in dirt
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and dusts which may be inspired or inadvertently ingested.
General widespread contamination of the environment by lead
occurs through deposit of airborne lead directly in water, and on
streets and other paved areas from which some will be washed into
waters. Airborne lead also is deposited in relatively high
amounts on plants, along heavily travelled roads, and in lesser
concentrations but over vast areas more distant from highways.
Reduction of_lgadmin_gasoline will.r_therefore^_resultin_reduced
exposure of maru both directly from^reduction^in atmospheric
leadj. and indirectly from reductjon^of lead_in_dirt^dust£ and
at least to a minor extent^ on and in foods.
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U,S, Environmental Protection Agency
Region 5, Library (PL-12J)
H West Jackson Bputevard, 12th
Chicago. JL 60604-3590
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