EPA1S POSITION  ON THE HEALTH




    IMPLICATIONS_OF_AIRBORNE_LEAD
             PREPARED EY
U.S. ENVIRONMENTAL PROTECTION  AGENCY




          U01  M STREET, S.W.




      WASHINGTON, D.C.   20U60
           NOVEMBER 28, 1973

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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 Agency1s 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 Register (3)  and



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





                              1-2

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lead additives themselves.  This issue is discussed in a separate
paper entitled, "Lead in Gasoline, Impact of Removal 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 Rhoden, 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 itrpact 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. 3882-388U, February 23,




    1972.







2.  Federal Register, Vol. 38, No. 6; pp. 125U-1256, January 10,




    1973.







3.  Federal Register, Vol. 38, No. 6; pp. 1258-1261, January 10,




    1973.
U.  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.
                               1-5

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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 1,431,511 short



tons with  596,797 short tons  (4251) 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 II-l



summarizes lead consumption patterns in the United States for



1968 and 1971  (1,5) 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 IT-1, 352,61U  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  50X  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



shown to be substantial immediately adjacent to such surfaces.




 (8)







    In  1971, 26U,2UO 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 10y> 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.



This contribution has been estimated to be about 0.0005 ug/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  (1U).  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 pg/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  (24) 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


concentrations of approximately 0.1-0.5pg/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

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for two to seven hours have averaged from 9.U to 23.6 pg/mj


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 with individual 24 hour peaks ranging up to 57.3


ug/m ^ (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  5655, 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 ug 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 iig of lead/liter



of rain which was approximately 40 times as high as that found in



rainwater at non-urban sites (34) .








    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
    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-UO
years and that no upward trend in lead levels in food is evident
    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."  (13) 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. 68U.








U.  Ibid., p. 68U.







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.
                               11-13

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8.  Comments submitted by the Ethyl Corporation to t.he



    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 #21U85-6013-RU-00, 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.








1U. Ibid. ,  pp. 11-13.
                              n-i4

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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. U: 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.
                            11-15

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23.  Darrow, O.K. and Schroeder, H.A., "Childhood Exposure to



    Environmental Lead," paper presented before the American



    Chemical Society, Chicago, 111.,  August 29, 1973.








2<*.  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.
                              11-16

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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.
                              11-17

-------
37.  Ibid., pp. 33-37.








38.  Ibid., pp. 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. 94:155-175, 1968.








10. Airborne  Lead in  Perspective,  op.cit.,  p. 189.








11. 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.







12. 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.








13. Ibid.,  p. 20.
                               11-18

-------
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 has 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 metal



or its compounds and from ingestion 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

-------
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 "jug/100g of blood" and ug/ 100ml of blood11 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.g.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 occurs.  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 jag



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




80pg/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 ug/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  ages 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  pg/100ml or had blood leads over



40 ug/lOOml with  urine leads exceeding 500 ug/24 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



difficulties, 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 been suggested by David, et al.  (9) that childhood



behavioral disturbances  such as hyperactivity may be associated



with blood lead levels between 25-55 >jg/100ml.  About half of the



hyperactive group  studied (28 of  5U) had blood leads between  25-



55  ug/100ml compared  to  less than one  third  (10 of  37)  in the



ccntrol group.  Both  the  hyperactive and the  control groups  were



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 Silbergeld,   et al.  (3U) 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  UO  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 pg/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 U-ll 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 UO-60 ug/100g  (22-25).  If increased urinary



ALA excretion is undesirable, it then follows that blood lead



levels above UO ug/100g 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  UO 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 of 40-60 ug/lOOg.  As blood lead levels increase above



i*0 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 HO



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 of Inorganic Lead Salts as Related to Estimates of Various Levels ol
and Remote




Type of Effects
Metabolic (accumu-
lation and excre-
tion of he me
precursors)

Functional injury:
Hcmatopoiesis



Kidney (renal
tubular
function)




Level 1:
No Demonstrable
in vivo Effect
Changing
ALAL)"



.
None



None





Level 11:
Minimal
Subclinical
Metabolic Effect
Slight increase in
urinary ALA
/ may be
present


None known



None known






Level 111:
Compensatory Biologic
Mechanisms Invoked
ALA, UCP. FEP
progressively increased




Shortened red-cell life-
span, rcliculocy
tosis(i)
(reversible)
•>





Level IV:
Acute Lead Poisoning


Mild Severe
ALA, UCP. FEP
increased 5- to 100 Told




Shortened red-cell life-span
and reticulocytosis
with or without anemia
(reversible)
Amino- Fancoru
aciduria, syn-
glycosuiia drome
(t) (re- (revers-
versible) ible)
F Absorption-Reecnl
Level V:
Lace Effects of
Chronic or Reciu-
- rent Acute LcaJ
Poisoning
Increased if excew.ic
exposure icircni.
but may noi tv in-
creased if CM.C-.MIC
exposure rcrmnc

Anemia (•)
(reversible)


Chronic ncphinpjtl:\ "
(permanent)



   Central nervous
      system

   Peripheral
      nerves
Clinical effects
None
None
                        None
                   None known
                   None known
                                           None known
Mild injury
(??? re-
versible)
Rare
Severe injury
(perma-
nent)
Rare
Severe injury b
(permanent)

Impaired condui
                                                             Nonspecific mild symp-
                                                                toms (may be due
                                                                in part to coexist-
                                                                ing diseases)
                                                            Colic, irri-
                                                                tability,
                                                                vomiting
Ataxia, stu-
   por, coma,
   convulsions
   (wrist, foot drup
   usually improve
   slowly, but may tv
   permanent)
Menial deficiency
   (ma/ be profounJt.
   seizure disorder.
   renal insufficiency
   (gout) (perma-
   nent)
Index of level of
recent or
current ab-
sorption:
Blood lead, <40
Mg/lOOgof
whole
blood
Urine lead -
(adults only).
pg/liter




40-60 50-100+ >80 >80
With anemia.
intercurrent disease:
50-100+
<80 <130 >|30 >130
(May be less in severe illness)

jn. in/



May be normal



Spontaneous
excretion may
normal









be

"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, D.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 turden. 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:  U43-449, 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

-------
IV.   Can_an_Acceptable 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 10-30ug/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 UOug/lOOg 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



ug/lOOg 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 40ug 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 ug/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



PBC.  Among children with blood lead levels  between 10-59



pg/lOOml,  55%  were observed to have FEP levels above 250



pg/lOOml.   In  contract, only  5% of children  with blood  leads



below  40  ug/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  40



ug/lOOg  (12).   The widespread prevalence  of  iron deficiency



anemia  among  the  population  at greatest risk from  lead  exposure



should  alsc be noted.   A  positive FEP  test  accompanied  by  a blood
                            IV-4

-------
lead below 40 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 HO pg/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  (1U),  lambs exposed to maternal



blood  lead  levels  of  3U  ug/lOOml  during gestation demonstrated



slowed learning  on a  visual discrimination task at 10-15  months



of  age.   This  deficit is consistent with  visual-perceptual



problems that  have been  noted in  children with  lead poisoning.



Extrapolation  of these  findings directly  to  man  is, however,



somewhat uncertain since a  blood  lead of  34  pg/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?
         What combinations of level and duration of exposure
        produce 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," Arner. 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.  Dobbing, 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., B. Davidow, V. F. Guinee, 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.








1U. 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-11

-------
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 man's 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 kncwn 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.)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 ug/lOOg 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 ^ig/100g) 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 500yg




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 40ug/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 (1U) .  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., UOug 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-UO 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




30-10 ug  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 (m3)  for a  "standard man"



 (weighing 70kg, 20-30  years  of  age,  175  cm tall,  and having  a



surface  area of 1.8 m *)  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 15-20m3of inhaled air daily.  As an



example, the amount of lead absorbed from breathing air



containing 1ug/m3of lead assuming 30% absorption and inhalation



of 20m3of 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 tOug 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



5.0ug/m3 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



exposed to airborne lead levels of 10.9ug/m3 and 3.2ua/m3for 23



hours a day in two separate experiments.  Average blood lead



levels among the men exposed to 10.9pg/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 3.2ug/m3 of air lead for 11 weeks increased from about



19 to 25pg/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/m3 and



Dr. Kehoe1s 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-



37pg/100ml in only a little over four months.








    The experiment in New York State at lead exposure levels of



3.2ug/m3 also showed that the men who had  been previously exposed



to airborne lead at 10.9ug/m3, responded differently to their



subsequent re-exposure, compared to subjects not  so  previously



exposed. (18) The previously  exposed men had consistently higher
                               V-8

-------
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


U.60, 2.U1, and 2.24 ug/m3respectively.  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

                          o
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 g  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.U and 457 meters from a turnpike (22,26).  The average outdoor



air lead levels at 33.a meters and 457 meters were 1.95 and 1.73



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 3for office workers in Starke, Florida, and



Barksdale, Wisconsin, to 3.06 for office workers and 6.10 ug/nr



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 ug/100 g in Barksdale to 2U.6 ug/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 frcm 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
                                                       o
for a "standard man", a person breathing 1 ug of lead/m  of air

would absorb a total of 6 ug daily from his respiratory tract and

a person breathing 3 ug of lead/m3 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 ug,

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
                                                            o
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  B) breathing 3 ug/m3 of lead in air and eating 220 ug of


lead daily, viz:
                                 V-14

-------
    Lead_lntake                 Subject_A







    Absorbed from air             6 ug              18 ug







    Absorbed from diet           M_US              22_jj3







    Total Daily  Lead



      Absorption                 <*0 ug              U0 U9







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/U the total daily air intake  (6rr? ) and about 40-



60% of an adult's total dietary lead intake  (130 ug) (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/U  teaspoon,  although



this may vary somewhat depending  on  its characteristics.   Since



these  dusts often  contain  1000-2000  pg/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 t»0 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 40 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 l/<4 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

-------
                             FIGURE V-1
       The average concentration  of lead in the  blood of subjects
       S.W., M.R.,  E.B.,  and I.F.  (from reference 12)
o
.08-
o
o
o
  «/>

  52 .06
.04

.02

 0
     I   I  I  I   I  I   I  I  I   I  I   I
        SUBJECT M.R.(1270Mg)
I  I   I  I   I  I.  I  I  I   I  I
  SUBJECT E.B.(2350Mg)
                                   SUBJECT S.VUMOpg)
     SUBJECT..F.(3270Mg»    CQNTROL pER|OD(300pg)
     l   l  I   I  I  I   I  l  l   I  I   I  l   l  l  l   I  '   l  l
                   I   I  I
   0    2    4    6    8   10   12   14   16    18   20
              TIME IN SUCCESSIVE PERIODS OF 28 DAYS
                                                       22   24

-------
                              FIGURE V-2

         Regression  of average blood  lead  versus time  in  a subject
         ingesting a total  of 600ug of dietary lead daily (adapted
         from  reference 12)
      45
o E
2 540
   ~
O O 2C
o o •"
Q P
o
z
LU
>
30
      25
                I
                   I
                        I
  I
      I
1
I
I
                                               •  •
A
Y
36.5  + 0.70IX-7.5)
      95% CONFIDENCE INTERVALS
           b = 0.17-1.23
                                         Y  = 24.9-37.6
                                          o
                           I
          I
              I
        I
                        5               10
                        TIME IN SUCCESSIVE 28 PERIODS
                                                  15

-------
                            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/nr)          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
^Assumes 30% absorption and 20m  daily respiration.

*Assumes 10% absorption of a daily dietary intake of 300 jjg
 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 jjg/100 g of whole blood with the consequent
 increased excretion of delta-aminolevulim'c 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/m J
Least(b)
Case
Highest(c)
Case
15.7 ng/m \  5.4 ug/m?
11.8 .yg/rri    4.0 ug/rn
+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 d:
            x 30% absorption
            x 17% absorption
            ; 37% 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
 49-60  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

-------
 6.   Goyer, R.A.,  and B.C.  Rhyne, "Pathological Effects of



     Lead," Int'l.  Rev.  Exp. Path., 1973, 12:pp. 1-77.







 7.   Ibid.







 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:11 Proceedings of the International Symposium on



     Environmental Health Aspects of Lead;11 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

-------
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.








2<*.   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.



     OAP 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.581-594.







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

-------
     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

-------
VI.   Lead Exposure from Dustfall







    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 (1-4) r 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 U68 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

-------
Philadelphia and dirt from playgrounds adjacent to those schools



routinely contained 0.2-0.3% lead, with levels greater than 1%



found at two locations (1U).  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 741.5 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

-------
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

-------
    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 U pg/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

-------
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

-------
                     o
of lead in air (5ug/mJ) 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 U


years of age had blood lead levels in excess of UOug/lOOg,  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

-------
    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-1910 homes had greater quantities of lead  in



housedust than post-1910 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

-------
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 HOug/lOOg)  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 UO 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-8

-------
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 H to 400 times higher than found in  the






                                VI-10

-------
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 4U,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
                              Vl-ll

-------
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 tOug/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

-------
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 <*4ug/ 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 fcr 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
jig/100 ml or more  (38).   In  1968 the  fraction of children with
blood  leads  in this range dropped to  3.6% and  in 1969 to 1.5%.
Figures for 1970 and 1971 were 2.1% and 2.3% resoectlvely.
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  4.1% of  children screened
that year had blood lead  levels of  50 ug/100  ml or above (42).
Thus,  though efforts  to  reduce  lead paint  exposure continued,  the
reported  frequency of  undue  lead exposure  but not  severe lead
                             VI-14

-------
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,UO).  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, D.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 UO ug/lOOg.



Blood lead determinations in this survey of 808 children showed
                             VI-15

-------
that 5.8% of all children tested had a blood lead of at least 40



ug/100g 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  (HH,H5) .








    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  (U6),  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, U9.3X were found  to  have blood lead  levels between



 UO-59  pg/100 ml  and  8.1% had blood  lead levels of  60 ug/100 ml



and above.   Children residing  100-200  feet and greater than 200



 feet  from  roajcr  roadways were  not  significantly different  from






                              VI-16

-------
each other.  Approximately 2551 of blood leads in both groups were



between 40-59 ug/100 ml and 3-5% were at least as high as 60



jig/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 10-59 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 2U,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

-------
    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. (H7) Correlation coefficients for these indices and rates



of excessive lead absorption  (blood lead of 60 ug/lOOg and above)



and elevated blood lead  (40 ug/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

-------
    In a study in Philadelphia, referred to earlier  (1U), 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 61U 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 qreat 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 9, 1973.

   pp. V-1U  -  V-19


3.   Ee Treville,  T.P.,  "Natural Occurrence of Lead,"

   Arch. Env.  Health, 8:212-221, February 1964


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," Trace Substances in Environmental  Health V.



   A  Symposium,  1972 pp.  129-1U2








 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. Darrow, D.K.  and Schroeder, H.A.,  "Childhood



   Exposure  to  Environmental 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








11.   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

-------
2«.  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 1U Illinois Cities of Intermediate Population,"



    JAMA:  221, p. 1175-1^79, September 1972








31.  Gilsinn, J.F., "Estimates of the Nature and Extent



      of Lead Paint Poisoning in the United States,"



      NBS Technical Note 7U6, December 1972








32.  Lin-Fu, J.S., "Vulnerability of Children to Lead



    Exposure 6 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,



    EPA, dated August 6, 1973








3U. 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 submitted



    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, D.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








UO. Personal communications from  H.  Sachs,  formerly Director,



    Chicago Lead Poisoning Program to Administrator, EPA,



    dated March 5,  1973  and June  15,  1973








HI. "Airborne Lead  in Perspective,"  op.  cit.,  p. 140
                             VI-29

-------
12.  Personal communication from H. L. Slutsky,



    Coordinator, Chicago Lead Poisoning Program to



    J. S. Lin-Fu, HEW, August 28, 1973.








U3.  Conn, R- H. and D. Anderson, "D. C. Mounts Unfunded



    Program of Screening for Lead Poisoning," HSMHA



    Health Reports, 86:<*09-U13, May 1971.








UU.  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.







U5.  Gilsinn, J.F., Estimates of the Nature and Extent



    of Lead Paint Poisoning in the United States,



    National Bureau of Standards  Technical Note 7U6,



    December 1972.








£16. 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.








U7. 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 ijniversity and the New Jersey College of



Medicine and Dentistry, Newark, New Jersey.



Prepublication draft.
                           VI-31

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VII.   Extent of Lead Exposure Among the General_Pogulation






    In section IV, it was stated that .determination of lead in



blood is at present the test 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 20-50pg/100g or



higher  (3,1,6-9).  The few data on commercial drivers (H, 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-U)  (See Table VTI-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

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                                    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.
12,
15.0
44.0
67.0
.3
,5
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 tig/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                      U


Phiadelphia Males (4)
  Urban                                66                      J's
  Suburban                             23                      u


Composite  (3)
  Urban                                833                      Z.7
  Suburban                             162                      u
 *0nly those  above  40 ug/lOOg.

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                                 TABLE VI1-3

        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
Aurora, 111.
Springfield,
Peoria, 111.
E. St. Louis
Decatur, 111
Joliet, 111.
Rock Island,
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)
(12)
 (13,14)
 111.  (13,14)
 (13,14)
,  111.  (13,14)
.  (13,14)
 (13,14)
 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
1,152
2,309
449
670
387
376
793
383
285
298
103
226
264
1,225
1,339
1,821
1,200












(all ages)
(2 years)
















  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
         24.3
         30.1
         31.3
         24.7
         12.2
         24.
         21
         11
         12,
         16.4
         17.0
         22.
         23.
         39.
.3
.1
.4
.6
                                                            .7
                                                            .7
                                                            .2
                                                         19.5

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                       REFERENCES
1.   Subclinical  Lead Poisoning;  Editorial;  Lancet;  1:87, January 1973

2.   Tepper, 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. Pub!. 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

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VIII.  SummarY_and_Cgnclusions







                             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,U31,51U 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



26U,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

-------
data, 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  UO  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 pg/lOOg as  indicators of lead intake that should be  prevented.



The UO 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

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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/rn^ 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

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    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





                             VIII-5

-------
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 *0wg/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
                             VIII-6

-------
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
                                VIII-7

-------
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 roadsr and in lesser



concentrations but over vast areas more distant from highways.



Reduction gf_lead_in_qasQline will, therefore^_result_in_reduced



exposure of man, both directly^from reduction in atmospheric



lead^ and indirectly from reductign_of_lead_jri dirt^ dust, and



at least to a minor extent^ on_and in foods.
                                 VIII-8

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