REDUCING LEAD IN DRINKING WATER:
            A BENEFIT ANALYSIS
               Ronnie Levin
Office of Policy, Planning and Evaluation
  U.S. Environmental Protection Agency
            EPA-230-09-86-019


            Draft Final Report
              December 1986
          (revised Spring 1987)

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                       ACKNOWLEDGEMENTS
    Many people contributed to the publication of this document:

    This analysis would never have been undertaken without
Joel Schwartz.

    This document would not have been published without the help
and encouragement of Jeanne Briskin and Michael B. Cook.

    Much appreciation also to J. Michael Davis (ECAO/ORD),
Brendan Doyle (OPA/OPPE), Lester Grant (ECAO/ORD),
Peter Karalekas (Region I), Peter Lassovszky (ODW/OW),
James W. Patterson (Illinois Institute of Technology),
Michael Schock (Illinois State Water Survey), and Ethel Stokes
(EPA) — who consistently provided more help than they ever
wanted to.  Thanks also to Gene Rosov (WaterTest Corporation).

    Finally, special thanks to the many people who repeatedly
reviewed successive drafts of this report.

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                               TABLE OF CONTENTS
                                                                           PAGE
CHAPTER I:  INTRODUCTION


  I.A.  BACKGROUND INFORMATION

  I.E.  SUMMARY OF REPORT

    I.B 1.  The Occurrence of Lead in
            Public Drinking Water

    I.B.2.  Benefits of Reducing Children's
            Exposure to Lead

    I.B.3.  Blood-Pressure-Related Benefits
            and Other Adult Health Effects

    I.B.4.  Benefits of Reduced Materials Damage

    I.B.5.  Summary of Annual Benefits of Reduced
            Lead in Drinking Water

  I.C.  BOSTON CASE STUDY
1-1

1-2

1-5


1-10


1-16


1-19

1-22


1-25
CHAPTER II:  OCCURRENCE OF LEAD IN DRINKING WATER


  II.A.  SOURCES OF LEAD IN DRINKING WATER                                 II-2

    II.A.I.  Variables Affecting Lead Levels in Drinking Water             II-3

       II.A.I.a.  Key Water Parameters Affecting the Solubility of Lead    II-4

       II.A.l.b.  Lead Solder            •  •                                II-6

       II.A.l.c. -Lead Pipes                                               11-10

       II.A. l.d.  Other Potential Sources of Lead                          11-10

       II.A.I.e.  Other Factors Relating to Lead Contamination Levels      11-12

       II.A.l.f.  Summary                                                  11-13

    II.A.2.  Prevalence of Lead Materials in Distribution Systems          11-14

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                                 Table of Contents


                                                                           PAGE

  II.B.  DATA ON THE OCCURRENCE OF LEAD IN DRINKING WATER                  11-16

    II.B.I.  Patterson Study/Culligan Data on Tap Water                    11-18

       II.B.I.a.  Consistency with Other Data                              11-21

       II.B.l.b.  Potential Biases in the Data                             11-25

       II.B.I.e.  Alternative Analysis of Potential Exposure
                  to Lead in Drinking Water                                11-32

    II.B. 2.  Lead Contamination in New Housing                             11-38

  II.C.  ESTIMATED EXPOSURE TO LEAD IN U.S. TAP WATER                      11-41

    II.C.I.  Uncertainties and Assumptions in the Analysis                 11-42

    II.C.2.  Calculations of Exposure to Lead in Drinking Water            11-54

       II.C.2.a.  Estimate of Exposure to Lead in Drinking Water
                  to Inhabitants of New Housing                            11-55

       II.C.2.b.  Estimate of Exposure to Lead in Drinking Water
                  to Inhabitants of Older Housing                          11-57

       II.C.2.C.  Total Estimated Exposure to Lead in Drinking Water       11-58



CHAPTER III:  BENEFITS OF REDUCING CHILDREN'S EXPOSURE TO LEAD
  III.A.  PATHOPHYSIOLOGICAL EFFECTS

    III.A.l.  Effects of Lead on Pyrimidine Metabolism

    III.A. 2.  Effects on Heme Synthesis and Related
              Hematological Processes

       III.A.2.a.  Mitochondrial Effects

       III.A.2.b.  Heme Synthesis Effects

    III .A. 3.  Lead's Interference with Vitamin D Metabolism
              and Associated Physiological Processes
III-6

III-ll


III-ll

111-12

111-12


111-13

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                             Table of Contents
  III.A.4.  Stature Effects

      III .A.4.a.  Effects of Lead on Fetal Growth

      III.A.4.b.  Effects of Lead on Post-Natal Growth

      III.A.4.C.  Summary of Stature Effects

III.B.  NEUROTOXIC EFFECTS OF LEAD EXPOSURE

  III.B.I.  Neurotoxicity at Elevated Blood-Lead Levels

  III.B.2.  Neurotoxicity at Lower Blood-Lead Levels

      III.B.2.a.  Cognitive Effects of Lower Blood-Lead Levels

  III.B.3.  The Magnitude of Lead's Impact on IQ

III.C.  FETAL EFFECTS

  III.C.I.  Assessing the Benefits of Reduced
            Fetal Exposure to Lead

III.D.  MONETIZED ESTIMATES OF CHILDREN'S HEALTH BENEFITS

  III.D.I.  Reduced Medical Costs

  III.D.2.  Costs Associated with Cognitive Damage

     III.D.2.a.  Compensatory Education

     III.D.2.b.  Effect Upon Future Earnings

  III.D.3.  Summary of Monetized Benefits

11 I.E.  VALUING HEALTH EFFECTS:  CAVEATS AND LIMITATIONS

III.F.  SUMMARY OF ANNUAL MONETIZED AND NON-MONETIZED
        CHILDREN'S HEALTH BENEFITS
 PAGE


 111-17

 111-18

 111-20

 111-26

 111-28

 111-28

 111-31

 111-34
111-42

111-44


111-49

111-50

111-54

111-55

111-56

111-60

111-62

111-67

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                                Table of Contents
CHAPTER IV:  HEALTH BENEFITS OF REDUCING LEAD:  ADULT ILLNESSES
                                                                              PAGE
  IV.A.  THE RELATIONSHIP BETWEEN BLOOD LEAD LEVELS AND BLOOD PRESSURE        IV-2

    IV.A.I.  Epidemiological Studies of Blood Lead Levels                     IV-3
             and Hypertension

       IV.A.l.a.  Occupational Studies                                        IV-4

       IV.A.l.b.  Observational Studies                                       IV-5

       IV.A.l.c.  Population Studies                                          3V-7

    IV.A. 2.  Mechanisms Potentially Underlying
             Lead-Induced Hypertension Effects                                IV-16

       IV.A.2.a.  Role of Disturbances in Ion Transport by Plasma Membranes   IV-17

       IV.A.2.b.  Role of Renin-Angiotensin in Control of Blood Pressure      IV-18
                  and Fluid Balance

       IV.A.2.C.  Effects of Lead on Vascular Reactivity                      IV-22

       IV..A.2.d.  Effects of Lead on Cardiac Muscle                           IV-23

       IV.A.2.e   Summary of Lead-Related Effects on the                      IV-25
                  Cardiovascular System

    IV.A. 3.  Cardiovascular Disease Rates and Water Hardness                  IV-26

       IV.A.3.a   Studies of Cardiovascular Disease and Water Hardness        IV-27

       IV.A.3.b.  Lead/ Soft Water and Cardiovascular Disease                 IV-30

    IV.A.4.  Benefits of Reduced Cardiovascular Disease:
             Reductions in Hypertension and Related Morbidity and Mortality   IV-32

       IV.A.4.a.  Hypertension                                                IV-35

       IV.A.4.b.  Myocardial Infarctions, Strokes, and Deaths                 TV-35

  IV.B.  LEAD'S EFFECTS UPON REPRODUCTIVE FUNCTION                            IV-40

    IV.B.I  Estimating the Population At-Risk for
            Female Reproductive Effects                                       IV-43

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                                Table of Contents
  IV.C.  MONETIZED ESTIMATES OF ADULT HEALTH BENEFITS:
         REDUCED CARDIOVASCUIAR DISEASE RISK IN MEN

    IV.C.I. Hypertension

    IV.C.2. Myocardial Infarctions

    IV.C.3. Strokes

    IV.C.4. Mortality

    IV.C.5. Summary of Annual Monetized Benefits
            of Reduced Cardiovascular Disease

  IV.D.  VALUING HEALTH EFFECTS: CAVEATS AND LIMITATIONS

  IV.E.  SUMMARY OF ANNUAL MONETIZED AND NONMONETIZED ADULT HEALTH
         BENEFITS OF REDUCING EXPOSURE TO LEAD IN DRINKING WATER
PAGE

IV-45

IV-46

TV-47

IV-51

W-53


IV-54

IV-56


IV-60
CHAPTER V:  BENEFITS FROM REDUCED MATERIALS DAMAGE
  V.A.  THE CHARACTERISTICS OF AGGRESSIVE WATER

    V.A.I.  Parameters of Water Affecting Corrosivity

    V.A. 2.  The Electrochemistry of Corrosivity

    V.A.3.  Types of Corrosion

    V.A.4.  Corrosion Indices

    V.A.5.  Plumbosolvency and Other Factors
            Determining Lead Levels in Drinking Water

  V.B.  DAMAGE TO PUBLIC SYSTEMS FROM INTERNAL CORROSION
                                         /
    V.B.I.  Occurrence of Corrosive Water in the United States

    V.B.2.  Corrosion Damage

    V.B.3.  Estimating the Annual Costs of Corrosive Water

    V.B.4.  Monetized Benefits of Reduced Corrosion Damage


BIBLIOGRAPHY

APPENDIX A:  BOSTON CASE STUDY
V-4

V-5

V-8

V-9

V-10


V-12

V-15

V-15

V-20

V-22

V-29

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CHAPTER I:
                             LIST OF TABLES
                                                                       PAGE
    TABLE  1-1    Substances Included in the 1985 Proposed
                  National Primary Drinking Water Regulations
                                                      1-3
    TABLE  1-2    Estimates of Annual Per Capita Corrosion
                  Damage

    TABLE  1-3    Summary of Estimated Annual Monetized
                  Benefits of Reducing Exposure to Lead
                  from 50 ug/1 to 20 ug/1 (1985 dollars)
                  for Sample Year 1988

    TABLE  1-4    Summary of Estimated Annual Non-Monetized
                  Benefits of Reducing Exposure to Lead from
                  50 ug/1 to 20 ug/1 for Sample Year 1988
                                                      1-21
                                                      1-23
                                                      1-24
CHAPTER II:
   TABLE  II-l
Distribution of Culligan Data
•{Patterson, 1981)
 11-22
   TABLE  II-2
Municipal Water Samples and Population
Percentages from Culligan/Patterson Study
(Patterson, 1981)
11-30-31
   TABLE  II-3
Lead Contamination Levels in Tap Water by
Age of Plumbing (Field Studies)
 11-39
   TABLE  II-4
Percentages of Samples Exceeding 20 ug/1
of Lead at Different pH Levels, by Age
of House
 11-44

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CHAPTER III:
                            LIST OF TABLES
                                                                   PAGE
   TABLE   III-l
 Blood Lead Levels of Children in
 the United States 1976-80
III-8
   TABLE   III-2
 Percent of Children Requiring
 Chelation Therapy
                                                                   111-52
   TABLE   III-3
 Estimated Annual Benefits of
 Reduced IQ Damage by Using
 Changes in Expected Future Lifetime
 Earnings for Sample Year 1988
                                                                   111-59
   TABLE   III-4
 Monetized Annual Benefits of Reducing
 Children's Exposure to Lead Using
 Alternative Methods for Sample Year 1988
                                                                   111-61
   TABLE   III-5
 Summary of Annual Monetized and
 Non-monetized Children's Health
 Benefits of Reducing Lead in Drinking
 Water for Sample Year 1988
                                                                   111-68
CHAPTER IV:
   TABLE   IV-1    Benefits of Reducing Strokes
                                                 IV-52
   TABLE   IV-2
Summary of Annual Monetized Blood-
Pressure Related Benefits of Lowered
MCL for Sample Year 1988
   TABLE   IV-3
Summary of Annual Monetized and Non-
Monetized Health Benefits of Lowered
MCL for Sample Year 1988
 IV-62
CHAPTER V:
   TABLE   V-l     Estimate of Annual Per Capita Corrosion Damage  V-30

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CHAPTER III:
                           LIST OF FIGURES
                                                                 PAGE
   FIGURE III-l   Multi-Organ Inpacts of Lead's Effects
                  on the Heme Pool
III-2
   FIGURE III-2   Sunsrary of Lowest Observed Effect
                  Levels for Key Lead-induced Health
                  Effects in Children
III-3
   FIGURE III-3   Relationship of Blood Lead Level to
                  Weight in Children Aged 0 to 7
111-24
   FIGURE III-4   Relationship of Blood Lead Level to
                  Height in Children Aged 0 to 7
111-25
   FIGURE III-5   Flow Diagram of Medical Protocols for
                  Children with Blood Lead Levels above
                  25 ug/dl
111-51
CHAPTER IV:
   FIGURE  IV-1   Adjusted Rates of Death and Heart Attacks
                  versus Blood Pressure:   Frandngham Data
IV-37
CHAPTER V:
   FIGURE  V-l    1962 U.S. Geological Survey of Water
V-17

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                            CHAPTER I

                           INTRODUCTION


     This chapter, which provides an overview of the report,

consists of three parts:  a background of the regulation of lead

under the Safe Drinking Water Act, a summary of this analysis of

the benefits that could result from a reduction in the amount of

lead permitted in U.S. drinking water, and a summary of a case

study of the costs and benefits of reducing lead levels in drinking

water in the City of Boston.


I.A. Background

     The Safe Drinking Water Act (SDWA), passed by the U.S.

Congress in 1974, requires the U.S. Environmental Protection

Agency (EPA) to protect public health by setting drinking water

standards for public water supplies.*  Two levels of protection

are described in the SDWA.  Primary drinking water regulations,

applicable only to public water systems, control contamination

that may have an adverse effect on human health by setting

either a maximum contaminant level (MCL) or a treatment technique

requirement.  Secondary drinking water standards are non-enforce-

able recommendations concerning the aesthetic quality of drinking

water, e.g., taste or smell.

     The National Primary Drinking Water Regulations (NPDWR)

were first promulgated at the end of 1975.  EPA revises those

regulations by setting maximum contaminant level goals (MCLGs)
*  Defined in the Act as water systems serving 25 or more people
   or having at least 15 service connections.

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                                1-2


and related MCLs.  MCLGs are non-enforceable health-based goals,.

intended to protect against known or anticipated adverse health

effects, with an adequate margin of safety.  MCLs are enforceable

limits, to be set as close as feasible to the MCLG; feasibility

includes cost and technological constraints.  MCLs are proposed

at the same time as the MCLGs.

     On November 13, 1985, EPA proposed National Primary Drinking

Water Regulations (NPDWR) to set MCLGs for 28 synthetic organic

chemicals, 11 inorganic chemicals, and 4 microbiological parameters

in drinking water; these substances are listed in Table 1-1.  The

proposed MCLGs for probable human carcinogens were set at zero, and

MCLGs for other substances were based upon chronic toxicity and

other data.

     Lead is included among the inorganic substances proposed for

regulation in the NPDWR.  The current MCL for lead is 50 micrograms

of lead per liter of drinking water (ug/1);* the proposed MCLG is

20 ug/1.

     The 1986 Amendments to the Safe Drinking Water Act contain a

provision banning the use of materials containing lead in public

water supplies and in residences connected to public water supplies,

States have until June 1988 to begin enforcing this ban.


I.E. Summary of Report

     This analysis estimates some of the benefits that could result

from reducing exposure to lead in community drinking water supplies,
*  This is equivalent to and can be stated alternatively as 0.05
   milligrams per liter (mg/1), 0.05 micrograms/gram (ug/g), or
   50 parts per billion (ppb).

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                                      1-3
TABLE 1-1.  Substances Included in the 1985 Proposed National
            Primary Drinking Water Regulations (Maximum Contaminant
            Level Goals)	
A.  Synthetic Organic Chemicals

    1.  Acrylamide                              13.
    2.  Alachlor                                14.
    3.  Aldicarb, Aldicarb sulfoxide and
        Aldicarb sulf one                        15.
    4.  Carbofuran                              16.
    5.  Chlordane                               17.
    6.  Dibrcmochloropropane                    18.
    7.  o-,m-Dichlorobenzene                    19.
    8.  cis- and trans-1,2 Dichloroethylenes    20.
    9.  1,2-Dichloropropane                     21.
    10. 2,4-D                                   22.
    11. Epichlorohydrin                         23.
    12. Ethylbenzene                            24.

B.  Inorganic Chemicals

    1.  Arsenic
    2.  Asbestos
    3.  Barium
    4.  Cadmium
    5.  Chromium
    6.  Copper
    7.  Lead
    8.  Mercury
    9.  Nitrate arid Nitrite
    10. Selenium

C.  Microbiological Parameters

    1.  Total Coliform Bacteria
    2.  Turbidity
    3.  Giardia
    4.  Pathogenic Viruses
Ethylene-dibromide
Heptachlor and Heptachlor
epoxide
Lindane
Methoxychlor
Monochlorobenzene
Polychlorinated biphenyls
Pentachlorophenol
Styrene
Toluene
Toxaphene
2,4,5-TP
Xylene

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                                1-4


These benefits are probably much greater than those attributable to

just reducing the MCL for lead, but do reflect benefits attainable

with reduced exposure to lead through changes in the MCL coupled

with changes in EPA's monitoring requirements or other efforts to

reduce exposure to lead from drinking water.

     There are two primary categories of benefits evaluated in this

paper:  the public health benefits of reduced lead exposure (Chap-

ters II and IV) and reduced materials damages (Chapter V) relating

to the phenomenon of lead's presence in drinking water — as a cor-

rosion by-product.  In addition, because the calculation of health

benefits depends on the extent of human exposure, another chapter

(Chapter II) presents the available data on the occurrence of lead

in public water supplies, and presents estimates of the population

exposed to drinking water exceeding the proposed MCLG of 20 ug/1.

In assessing the benefits of the proposed reduced lead standard,

this analysis assumes that EPA will act to reduce lead levels in

tap water, as well as to maintain the current high quality of water

leaving the treatment plant.  It also relies upon and is sensitive

to assumptions about drinking water use and consumption patterns.

     This analysis estimates the annual benefits for one sample

year, 1988, of lowering the amount of lead permitted from 50 ug/1

to 20 ug/1.  That one year was chosen because environmental lead

levels will have stabilized following EPA's 1984 phasedown of lead

in gasoline.*
    Specifically, this analysis measures effects given the condi-
    tions on January 1, 1988, when EPA's proposed ban on leaded
    gasoline will not yet have taken effect.  However, even if EPA
    promulgates that ban, the estimates in this report will not
    change significantly.

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                               1-5



     For comparability, all monetary values are expressed in

constant 1985 dollars.*  The population baseline is the 219.2

million people served by community water systems.



I.B.I. The Occurrence of Lead in Public Drinking Water


     Lead occurs in drinking water primarily as a corrosion by-


product; its sources are the materials used in the distribution


and residential plumbing systems (cf sources as diverse as the


US-EPA Air Quality Criteria Document for Lead, 1986; Craun and


McCabe, 1975; Kuch and Wagner, 1983; Department of the Environment,


1977; etc).  Water leaving the water treatment plant is usually


relatively lead-free.  However, pipes and solder containing lead

are corroded by water, and lead levels at the user tap are often


much higher than those found at the treatment plant.  While the


presence of lead service pipes is relatively restricted geographi-

cally in the United States, the use of lead solder (and flux) is

ubiquitous.  And the combination of copper pipes with solder


containing lead found in most residences can result in high lead

levels** in first drawn water that has been in contact with the

pipe for a period of time — levels exceeding the current MCL,

even with fairly non-corrosive waters (e.g., Nielson, 1976).  In

particular, newly-installed solder is easily dissolved, and

people living in new housing, or in older housing but with new
*   The 1986 Economic Report of the President to Congress (Table
    B-4).                                            	


**  This results from galvanic corrosion, which is the corrosion
    that occurs when 2 metals, with different electro-chemical
    potential, are in the same environment.

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                               1-6

plumbing, are especially at risk of high levels of lead in the
drinking water (Sharrett et al., 1982a; Murrell, 1985).  Lead
concentrations in fully flushed water typical of dis€ribution
system water, even under corrosive conditions and with new solder,
are generally below 50 ug/1 and usually below 20 ug/1.
     Because lead occurs generally as a corrosion by-product in
U.S. community water supplies, levels in fully-flushed water and in
distribution water are typically low.  Exposure to lead, however,
is from tap water that can contain significant amounts of lead.
The estimate of the occurrence of lead in drinking water, therefore,
is based upon data collected and analyzed for EPA's Office of
Drinking Water in 1979-81.  These data portray lead levels partly
flushed (30 seconds), kitchen tap samples collected by the Culligan
water-softening company.*  J. Patterson of the Illinois Institute
of Technology analyzed the data.  Current evidence indicates that
these samples are more representative of consumed water than are
the fully-flushed samples taken in compliance with EPA's monitoring
regulations.  The Ciilligan data indicate that 16 percent of
partly flushed water samples could exceed an MCL of 20 ug/1 at
the kitchen tap.  The findings from this data source are consistent
with other analyses of the occurrence of lead in tap water and
with studies of lead leaching rates in corrosive and non-corrosive
waters.
     To this must be added the inhabitants of housing built within
the past 24 months and that have plumbing materials containing lead.
*   The use of company names and the presentation of related data
    does not constitute endorsement of their services.

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                               1-7


Many studies have shown that new solder can release significant

amounts of lead into water, even exceeding the current MCL of 50

ug/1 (e.g., Sharrett et al., 1982a; AWWA-DVGW Cooperative Research

Report, 1985).  While corrosive waters have the highest lead

levels, relatively non-corrosive waters can also leach significant

amounts of lead.  The highest lead contamination levels occur

with the newest solder (i.e., during the first 24 months following

installation), but those levels decline and are generally not

elevated beyond five years (e.g., Sharrett et al., 1982a;

Lassovszky, 1984).

    There were 1.7 million new housing starts and permits in the

United States during 1983 and 1.8 million in 1984.*  Construction

data show that housing typically takes six months to a year from

permit to potential occupancy, so there are currently about 3.5

million new housing units (i.e., < 24 months).  The Statistical

Abstractofthe United States (1985; Table 58) indicates that

the average household contains 2.73 individuals.  Multiplied

together, a total of 9.6 million people currently live in new

housing.

     However, not all of these people are served by community water

supplies:  of the current (1985) U.S. residential population of

over 240 million, 219.2 million are served by community water

systems and this analysis only addresses that population.  In

addition, data from the plumbing supply industry show that about
*   Survey of Current Business, U.S. Department of Commerce -
    Bureau of Economic Analysis, 1985; Table on New Housing
    Construction.

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                              1-8


8 percent* of new plumbing is plastic, so 92 percent of the

population has metal pipes.  Therefore, the number of people at

risk of high lead levels from new solder in new housing is:

                   219 mil
         9.6 mil x 240     x .92 = 8.1 million.

     To calculate the risk to inhabitants of older housing, subtract

the number in new housing (8.8 million)** from the total served by

community water systems (219.2 million); that indicates that 210.4

million people live in older homes.  Based upon the Culligan data,

16 percent of them (33.7 million) are at-risk of high lead levels

from partly flushed water at the kitchen tap.  Combining the data

from Culligan on lead levels in older housing with the new housing

exposure estimates indicated that 41.8 million people using public

water supplies currently may be exposed to some water that exceeds

the proposed MCL of 20 ug/1; we round this to 42 million.

     This may be a low estimate

        0  because it does not include the potential exposure
           of occupants in housing built within the past 2-5 years
           (who also probably remain at greater risk of elevated
           lead levels);***

        0  because we have not included those who, while living
           in older housing, have recently had major plumbing
           repairs and so are also at risk of the potentially high
           lead levels associated with newly installed solder;
    This is the average of claims by the Plastic Pipe Institute
    presented in Mruk (1984) and of the Copper Development
    Association presented in Anderson (1984).
                          219 mil
**  Derived:   9.6 mil x  240
= 8.8 million people.
*** Inhabitants of 2-5 year old housing are not included in this
    analysis because it was not possible to eliminate them from
    the base and thus avoid double-counting.

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                               1-9


         0   because the  Culligan data represent water that is
            harder than  average, whereas high lead levels are
            often found  with soft waters;  and

         0   because the  data used are for partially flushed
            samples,  while  some people (especially children)
            may  consume  water that is closer to first-flush
            or standing  samples (which is  more likely to
            contain higher  concentrations  of lead).*

      In  addition,  we have  not included any  data from the estimated

60 million  people  served wholly or in part  by private and non-

community water  supplies.

      There  are uncertainties,  however,  concerning actual patterns

of drinking water  use and  the extent of plastic piping  in new

construction that  could reduce  the estimate.   Early  enforcement

of the Safe Drinking Water Act  ban on the use  of materials

containing  lead  in public water  supplies, enforceable  in June

1988, could also decrease exposure  to lead  from drinking water.

     The assumptions on the relationship between water  lead  levels

and blood lead levels are taken  from the draft  (EPA) Water Criteria

Document for Lead  (1985), which  is based upon  the recommendations

in the Air Quality Criteria Document  for Lead  (US-EPA,  1986).

Those documents assume a linear  relationship, at  least at the

lower blood-lead levels typical of the United States, with dif-

ferent constants for children and adults relating first-flush water

lead levels to blood lead concentrations.  Those formulae are:
    Water standing in pipes has a greater opportunity for lead to
    leach into it and, therefore, is more likely to contain higher
    lead levels.   Many of the factors affecting lead levels in
    drinking water are discussed in Chapters II and V of this
    report.

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                              1-10


     (for children)1" PbB* = 0.16** x intake of lead from water

     (for adults) PbB* = 0.06** x intake of lead from water.


Alternative assumptions (e.g., those reasonably derived from the

results of Richards and Moore, 1982 and 1984) could imply that

exposure — and consequently benefits —may be underestimated,

possibly by several factors.

     The estimates of the health benefits associated with this pro-

posed rule rely upon data on the distribution of blood lead levels

in children and adults collected as part of the Second (U.S.)

National Health and Nutrition Examination Survey (NHANES II), a

10,000 person representative sample of the U.S. non-institutional-

ized population, aged 6 months to 74 years.  That data base is

available from the (U.S.) National Center for Health Statistics

and analyses of lead-related data from it have been published

before  (e.g., Annest et al., 1982 and 1983; Mahaffey et al.,

1982; Pirkle and Annest, 1984).

     This analysis- uses both point estimates and ranges of blood

lead levels associated with specific health outcomes.  Other EPA

analyses  (e.g., US-EPA, 1986a) use ranges exclusively.  Both

approaches are supported by the available data.


I.E.2.  Benefits of Reducing Children's Exposure to Lead

    Elevated blood-lead levels have long been associated with

neurotoxicological effects  and many other pathological phenomena:
   PbB
blood lead level
 ** These  constants have  a  unit  of micrograms-of-lead/deciliter-of-
   blood  per microgram-of-lead-in-water/day,  or  ug/dl per ug/day.

 t  This formula was  derived  from Ryu,  1983.   An  alternative estimate
   from the data  in  that paper  suggests  a  coefficient of about 0.4.

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                               1-11

 an article on lead's neurotoxicity was published as early as 1839,
 on anemia in the early 1930s,  on kidney damage in 1862, and on
 impaired reproductive function in 1860.  As noted in the Air
 Quality Criteria Document for Lead (US-EPA, 1986),  from an his-
 torical perspective, lead exposure levels considered acceptable
 for either occupationally-exposed persons or the general popula-
 tion have been revised downward steadily as more sophisticated
 bio-medical techniques have shown formerly-unrecognized biological
 effects,  and as concern has increased regarding the medical and
 social  significance of such effects.   In the most recent downward
 revision  of maximum safe levels  for children,  the Centers for
 Disease Control (CDC)  lowered  its definition of lead toxicity  to
 25  micrograms  of lead  per deciliter of blood (ug/dl,  the standard
 measure of blood lead  level) and 35 ug/dl of free erythrocyte
 protoporphyrin (FEP)..  AS evaluated in the Criteria  Document
 (1986), the present literature shows  biological effects  as  low
 as  10 ug/dl (for heme  biosynthesis) or 15  ug/dl (for  certain
 renal system effects and neurological  alterations);  indeed, a
 threshold has  not yet  been  found for  some  effects  (e.g.,  elevated
 levels  of  a potential  neurotoxin* or  stature effects, Angle et
 al., 1982;  Schwartz et  al., 1986).
     There  is  no convincing evidence that  lead has any beneficial
biological  effect in humans (Expert Committee on Trace Metal
Essentiality,  1983; and  included in the Criteria Document, 1986).
     Elevated blood-lead  levels have been linked to a wide range
of health effects, with particular concern focusing on young

*  ALA,  or aminolevulinic acid.

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                              1-12

children.  These effects range from relatively subtle changes
in biochemical measurements at 10 ug/dl and below, to severe
retardation and even death at very high levels (80-100 ug/dl).
Lead can interfere with blood-forming processes, vitamin D
metabolism, kidney function, neurological processes and repro-
ductive functions in both males and females.  In addition, the
negative impact of lead on cognitive performance (as measured by
IQ tests, performance in school, and other means) is generally
accepted at moderate-to-high blood-lead levels (30 to 40 ug/dl
and above), and several studies also provide evidence for possible
attentional and IQ deficits, for instance, at levels as low as
10-15 ug/1.  Changes in electroencephalogram readings, as another
example, have also been observed at these low levels.  For many
subtle effects, the data may represent the limits of detectability
of biochemical or other changes, and not necessarily actual
thresholds for effects.
     For children's health effects, two categories of benefits
were estimated monetarily:  1)  the  avoidance of  costs for medical
care for children exceeding the  lead toxicity level set by the
Centers  for Disease Control  (i.e.,  25 ug/dl, when combined with
FEP levels of > 35 ug/dl)  and  2)  the averting of costs due to
lead-induced  cognitive  effects.   Two alternative methods  for
valuing  the potential cognitive  damage resulting from exposure  to
lead were  developed.  The  first of  these  two  alternatives involves
assessing  the costs of  compensatory education  to address  some of
the manifestations  of  the  cognitive damage  caused by  lead as  a

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                               1-13

 proxy measure for the damage itself.  The second relates to one
 specific indication of that cognitive damage — potential IQ
 point loss, and includes a calculation of decreased expected
 future earnings as a function of IQ point decrement.  These esti-
 mates neither include many major categories of pathophysiological
 effects (e.g., renal damage), nor do either the medical costs
 or the compensatory education costs consider any lasting damage
 not reversed by medical  treatment or compensatory education.   These
 estimates also attribute few benefits to reducing lead levels in
 children whose blood lead levels would be below 25  ug/dl even in
 the absence of this  proposed rule.
      The estimate  of reductions  in  medical care expenses rely upon
 published recommendations (Piomelli et al.,  1984)  for  follow-up
 testing  and treatment  for children  with blood  lead  levels above 25
 ug/dl.   The costs  of such medical services and  treatment were
 estimated  at about $950  per  child over 25  ug/dl (1985  dollars).
 This  average reflects  both lower costs for most of  these children
 and much higher  costs  for the smaller  subset requiring  chelation
 therapy.
      The estimates for compensatory education assumed three years
 of part-time compensatory education (de la Burde and Choate, 1972
 and 1975) for 20 percent  of the  children above  25 ug/dl, averaging
 about $2,800 (1985 dollars) per  child  above that blood  lead level
 based upon data from the  U.S. Department of Education (Kakalik
et al., 1981).
     There is extensive literature examining the relationships
between IQ, educational levels attained, demographic variables and

-------
                              1-14


earnings (ICF, 1984).  The results of that literature were used to

estimate the effect of IQ point losses that can occur as a part of

the cognitive damage caused by lead exposure upon expected future

earnings: one IQ point can directly and indirectly affect earnings

by 0.9 percent.  The studies of cognitive damage presented in

the Air Quality Criteria Document for Lead (U.S. EPA, 1986) show

evidence that blood  lead levels of 15-30 ug/dl can be associated

with IQ losses of 1-2 points, blood lead levels of 30-50 ug/dl

can be associated with IQ losses of 4 points, and over  50'ug/dl of

blood lead  can correlate with losses of 5 points.  Data from  the

Census Bureau on expected future  lifetime earnings,  deferred  for  20

years* at a 5 percent real discount rate and  then annualized,  yield

estimated benefits  of avoided damage from reduced exposure to lead.

This  alternative method  for  valuing  some of  lead's cognitive  damage

indicated that society could save $1,040 per  child brought below  15

ug/dl;  $2,600 per  child  brought  below  30 ug/dl;  and  $2,850 per

child brought below 50 ug/dl by  reducing  lead in drinking water

 (1985 dollars).

      In sum, this  analysis  indicates that  the proposed rule  could

 produce benefits of $27.6 million annually in avoided medical

 expenses;  $81.2  million  per year in reduced compensatory education

 costs;  and $268.1  million per year in increased lifetime earnings,
 *  These costs are deferred because those suffering the effects are
    children and will not enter the work force for up to 20 years.
    Obviously, using the largest deferral period (20 years) reduces
    the value of the benefit and reduces the benefit estimate,
    whereas 8- or 10-year-old children may begin working within_8
    years and so would have a much shorter deferral period.  This
    biases the estimates downward slightly.

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                               1-15


based upon  sample year  1988;  these  estimates  are  in  1985  dollars.

Note that compensatory  education  and  affected earnings  are  alter-

native methods  for valuing aspects  of the  cognitive  damage  caused

by lead.*

     In addition, benefits potentially derived by decreasing the

incidence of two other  categories of  health effects  (lead's adverse

effect upon children's  growth and fetal effects) were not estimated

in dollar terms.  Assuming that pregnant women are distributed

proportionately throughout the country, data  from the Census Bureau**

on birth rates and demographic distributions  indicate that  24 per-

cent of the total population is women of child-bearing  age  (15-44)

and that the birth rate is 67.4 births per 1,000 women  aged 15-44.

Therefore,

          41.8 million x 24% x 67.4 per thousand = 680,000.

It is estimated that this proposed  rule could  prevent 680,000

fetuses from being exposed to elevated lead levels.  The fetal

effects are particularly important, because several  recent  studies

have shown that lead exposure within the normal range (6-2'0 ug/1)

can be associated with various negative pregnancy outcomes  (such as

early membrane rupture and even miscarriages,  e.g., Moore,  1982;

Wibberly et al., 1977), and with low birth weight, inhibited post-

natal growth and development (e.g., Bornschein, 1986; Bellinger,

1985 and 1986; Dietrich et al., 1986).  In addition, this proposed

rule could prevent 82,000 children from risk of growth effects.
*   This also biases the results downward because there is a strong
    rationale for considering these effects as additive.

**  Statistical Abstracts (1986), Tables 27 and 82.

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                             1-16

I.E.3. Blood-Pressure-Related Benefits and Other Adult
       Health Effects
   Lead has long been associated with elevated blood pressure, but
until recently most of the studies have focused only on hyperten-
sion and relatively high lead levels typically found only in those
occupationally exposed to lead.  Several recent studies, however,
(e.g., Pirkle et al., 1985; Harlan et al., 1985; Pocock, 1984 and
1985) , have found a continuous relationship between blood lead and
blood pressure.  These studies provide evidence for a small (com-
pared to other risk factors) but robust relationship after control-
ling  for numerous other factors known to be associated with blood
pressure.  Experimental animal studies in several species of rats
and pigeons also provide evidence of a relationship between
moderate blood-lead levels and increases  in blood pressure.
      To calculate these benefits, logistic regression equations
were  used  to predict how reducing exposure to  lead  in drinking
water would affect the number of hypertensives  in the U.S. popu-
lation.  These estimates cover only males aged  40 to 59, because
the effect of lead on blood pressure appears to be  stronger for men
and because the correlation between blood pressure  and  age  is much
smaller in this age range, reducing the potential for confounding
due  to the correlation between blood  lead and  age.  The estimates
rely  upon  1) site-adjusted coefficients from analyses of the  NHANES
II  data relating  blood lead  levels  to  increases in  blood pressure*
and  2) coefficients relating  blood  pressure  increases to more serious
 *  The  specific coefficients and the basis for their derivation are
   described in the Addendum to the Criteria Document,  1986, which
   is included in volume 1 of that publication.

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                                 1-17

 cardiovascular disease outcomes, based on data  from  the  Framingham
 Study  (McGee et al., 1976) and  Pooling Project  (1976), as confirmed
 by Levy et al., 1984.
      Levy has demonstrated that the risk coefficients from the
 Framingham Heart Study, when coupled with the observed reductions
_ln blood pressure, smoking, and cholesterol in the U.S. population
 during the 1970s, correctly predicts the observed reductions in
 cardiovascular mortality in the overall population during that
 decade.  The Pooling Project showed that the Framingham coefficients
 adequately predicted cardiovascular outcomes (such as strokes and
 heart attacks)  in the other five large prospective heart studies
 performed  in the  U.S.  Therefore,  while caution is clearly warranted
 in view of the  limited  data on the effect of lowering blood lead
 levels  on  blood pressure,  use  of the  regression coefficients  from
 the  Framingham Study provide a reasonable basis by which  to predict
potential  changes  in cardiovascular outcomes associated with  blood
pressure changes  due to decreased  lead  exposure.
      Based upon this  information, reducing exposure to lead from
drinking water in  1988 could reduce the number  of  male hypertensives
(aged 40 to 59) by 130,000.  Using  estimates of  the costs of medical
care, medication, and lost wages, such a  reduction in hypertension
incidence would yield a value of $250 per year per case avoided  (1985
dollars).
     These estimates of how blood pressure reductions would affect
the incidences of various cardiovascular diseases  were based on
projections of changes in blood pressure as a result of the proposed
rule and estimates of the relationships between blood pressure and

-------
                               1-18

heart attacks, strokes, and deaths from all causes.  As noted
earlier, the latter estimates were derived from several large
epidemiological studies, primarily the Framingham study.  However,
because those studies  included very few nonwhites, the estimates
were further restricted to white males, aged 40 to 59.  Thus, the
benefits estimates do  not include middle-aged, nonwhite males.
     The basis of most of the medical  costs are the'cost-of-illness
estimates presented  in Hartunian et al.,  1981, which were  adjusted
in  three ways  to reflect current conditions.   First, we  inflated
them to 1985  dollars using  data from  the  1986  Economic Report of
the President to Congress.   Second, we adjusted  the  costs  to reflect
changes and improvements  in medical treatment, including the trip-
ling  in the incidence  rate  of coronary bypass operations that
occurred  between  1975  and  1982.   Third, Hartunian used a 6 percent
 real  discount rate to present-value future expenditures, while
 this  analysis uses a 10 percent real  discount rate.
      The value of reductions in heart attacks and strokes was based
 on the cost of medical care and lost wages for nonfatal cases.
 Expected fatalities from heart attacks and strokes  were included
 in the estimate of deaths from all causes.  That procedure yielded
 benefits of $65,000 per heart attack  avoided  and $48,000 per stroke
 avoided (1985 dollars) for  the 240 heart attacks and 80 strokes
 estimated  to  likely be avoided in 1988 because of this  proposed
 rule.  It  is  important to  note that  these estimates do  not  account
 for any reductions  in the  quality of life for the victims of heart
 attacks and  strokes (e.g.,  the partial paralysis  that afflicts
 many  stroke  victims).

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                                1-19




     Valuing reductions  in  the  risk of death  is difficult  and  con-


troversial, with a wide  range of estimates  in the  literature.


EPA's policy guidelines  (U.S. EPA, 1984c),  for example,  suggest  a


range of $400,000 to $7  million per statistical life saved.  Using


$1 million per case, the benefits of reduced  mortality dominate  our


estimates of total blood-pressure-related benefits? these  total


$240 million in 1988 for the 240 deaths estimated  as likely to


be avoided in that year.  Altogether, the monetized benefits of


reducing adult male exposure to lead in drinking water are


estimated to total $291.9 million per year  (in 1985 dollars),


using 1988 as a sample year.


     In addition, because lead  crosses the placental barrier and is


a fetotoxin, pregnant women exposed to lead are at risk of compli-


cations in their pregnancies and damage to the fetus.   (Fetal
                                   \
                                   i
effects are discussed above, under children1s health effects.)


While we have not monetized any of these  reproductive  effects,  as


noted above, 680,000 pregnant women per year probably  receive


water that exceeds the proposed standard  of 20 ug/1, and  would


benefit from the proposed rule.  Lead-induced effects  on  male


reproductive functions have also been  discussed in  the  scientific


literature but are not included in this report.



I.E.4. Benefits of Reduced Materials Damage
               !                  ~i       ~

    A third category of  monetized Benefits  relates  to the phenom-


enon of lead's presence  in drinking water:   it is a product of  the


corrosive action of water upon  the materials of the distribution


and residential plumbing.  For  the most part,  therefore,  treatment

-------
                              1-20


processes used to reduce high levels of lead in drinking water are

the same as treatment processes used to reduce the corrosion poten-

tial of the water.  Reducing corrosion damage will produce substan-

tial benefits to water utilities, their rate-paying customers, and

building owners.

     Published estimates of the costs of corrosion damage range

from $12 to $46 per person per year (1985 dollars), and are sum-

marized in Table 1-2.  Estimates of the costs that can be avoided

by corrosion control measures range from 20-50 percent of total

damage.  The point estimate of avoidable corrosion costs (i.e., the

benefits of corrosion control) is $8.50 per capita annually (1985

dollars).  For comparison, estimates of average corrosion treatment

costs range from under $1 per person per year (based upon the

experience in 18 cities currently treating their highly corrosive

waters) to about $5 per person per year (based upon the highest

treatment costs presented in the ODW cost report).*  As a point

estimate, we assumed per capita annual treatment costs of $3.80

(1985 dollars).

     Estimates of  the extent of corrosive water also vary.  A

commonly accepted  profile is that developed by the U.S. Geological

Survey  in the early 1960s, which identified the Northeast,

Southeast, and Northwest sections of the country as having the

softest and most corrosive waters  (Durfor and Becker,  1964a and
 *  The  range,  however,  is  quite  wide  and  highly  sensitive  to  system
   size.   These represent  average  costs.   In some  very  small
   systems (i.e.,  serving  25-100 people),  costs  may  be  many times
   higher.

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                               1-22


1964b).  The combined populations of those states are 67.7 million

people (1980 census).  Assuming that these areas are served

proportionately by community water systems,* 61.8 million people

would benefit from actions to reduce the corrosivity of their water,

That figure, multiplied by $8.50 per person, yields annual benefits

from reduced corrosivity of $525.3 million  (1985 dollars).


I.E.5.  Summary of Annual Benefits of Reduced Lead in
        Drinking Water

     This analysis of the benefits of reducing exposure to lead

in drinking water indicates that the monetized annual benefits

could  range from $926.0 to $1,112.9 million (1985 dollars) for

sample year 1988.  In addition, there are numerous health benefits

of reduced exposure  to  lead that are not monetized.  The annual

monetized benefits are  summarized  in Table  1-3,  and the non-

monetized benefits are  presented in Table 1-4.

     Based upon the  latest cost estimates used by the Office  of

Drinking Water** the projected benefits  exceed the  costs by about

4:1.   Expressed differently,  lowering the MCL to 20 ug/1 could

produce annual net benefits of about  $800 million  in  1988.

      It should be emphasized  that  considerable uncertainty  is

associated with these  estimated  benefits, uncertainties  derived

both from the  current  state of knowledge concerning lead health

effects  and the valuation of  avoiding such  effects.   Other
 *  Of the total population of about 240 million,  219.2 million
    people are served by community water systems.

 ** These calculations use preliminary EPA Office of Drinking
    Water cost estimates.  Costs and net benefits will be
    discussed more extensively in other documents associated
    with this proposed rulemaking.

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                                          1-23
 TABLE 1-3.   Summary of Estimated Annual Monetized Benefits of Reducing Exposure
 	to Lead from 50 ug/1 to 20 ug/1  (1985 dollars)  for Sample Year 1988
 Estimated population exposed  to drinking
 water exceeding proposed MCL
                                              42 million*
Children's health benefits

     -reduced medical costs

     -reduced costs of cognitive damage
      Method 1 - compensatory education
      Method 2 - decreased future earnings
TOTAL:
Method 1
Method 2
Adult health benefits (males only)

     -reduced hypertension savings
      (males, aged 40-59)

     -savings from fewer heart attacks
      (white males, aged 40-59)

     -savings from fewer strokes
      (white males, aged 40-59)

     -savings from fewer deaths
      (white males, aged 40-59)

TOTAL:

Materials benefits

     -benefits of reduced corrosion damage
                                              $27.6 million
 $81.2 million
$268.1 million

$108.8 million
$295.7 million
                                              $32.5 million


                                              $15.6 million


                                               $3.8 million


                                             $240.0 million


                                             $291.9 million



                                             $525.3 million
TOTAL ANNUAL MONETIZED BENEFITS

     -Method 1 - using compensatory education
     -Method 2 - using decreased future earnings

ESTIMATED ANNUAL COSTS

NET ANNUAL MONETIZED BENEFITS
                                             $926.0 million
                                           $1,112.9 million

                                             $230.0 million

                                     about   $800 million
* Total population served by community water systems:  219 million

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                                         1-24
TABLE 1-4. Summary of Estimated Annual Non-monetized Benefits of Reducing
           Exposure to Lead from 50 ug/1 to 20 ug/1 for Sample Year 1988

                                                   Reductions in Numbers
                                                     of People at Risk
Estimated population exposed to drinking
water exceeding proposed MCL
Children's health benefits"

   - children requiring medical treatment

   - loss of 1-2 IQ points
               4 IQ points
               5 IQ points

   - children requiring conpensatory education

   - children at risk of stature decrement

   - fetuses at risk

   - increased risk of hematological effects
42 million*



   29,000

  230,000
   11,000
      100

   29,000

   82,000

  680,000

   82,400
Adult health benefits

     -cases of hypertension
       (males, aged 40-59)

     -heart attacks
       (white males, aged 40-59)

     -strokes
       (white males, aged 40-59)

     -deaths
       (white males, aged 40-59)

     -(reduced risk to pregnant women
       ((women, aged 15-44)
       (same as fetuses
  130,000


      240


       80


      240


  680,000)
 * Total population served by community water systems:  219 million

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                                1-25


 analogous efforts to estimate benefits associated with reducing

 lead in drinking water may be useful in helping to judge how

 reasonable these present benefit estimates are.


 I.C.  Boston Case Study


       In the spring of 1986, Jonathan Jacobson analyzed the incre-

 mental costs and benefits to the City of Boston of reducing the

 lead MCL from 50 ug/1 to 10 ug/1 (Jacobson, 1986).*  That analysis,

 carried out as a masters thesis project at Harvard University,

 focused on Boston as a city with high potential for increased lead

 exposure via drinking water.

     Boston's water is highly corrosive:  it is relatively acidic

 (pH = 6.7)  and soft  (14 mg/1 as CaCO3), and has low alkalinity

 (Karalekas  et al.,  1975).   Boston also  has a large percentage of

 lead pipes  in service.   During  the 1970s,  several  studies found

 high lead  levels in  Boston's drinking water (e.g.,  Karalekas  et

 al.,  1975;  and several  internal studies conducted  by  the

 Massachusetts Water  Resources Authority and the [Boston]

 Metropolitan  District Commission).

      To  reduce the high lead  levels,  Boston began corrosion

 control  treatment.   Monitoring performed by EPA's Region  I from

 1975  to  1981  indicated  that  lead,  iron  and  copper levels  dropped

 significantly  (Karalekas et al.,  1982).  However, while lead

 concentrations generally decreased to below the current MCL of

 50 ug/1, additional  treatment will be necessary to comply with

 a lowered MCL.
* He assumed a lowered MCL of 10 ug/1 because that is the
  feasibility limit for current treatment and technology.

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                              1-26

     Jacobson analyzed the incremental annual costs and benefit's
of additional efforts by Boston to control further the corrosivity
of its water, using sample years 1988 and 1992, and estimating all
costs in 1985 dollars.  His analysis assumed the following:
        0  compliance will be measured by a standing "grab" sample,
           that is, a sample taken immediately after turning on
           the faucet at any random time during the day after an
           unknown period of standing;
        0  it will be impossible for every tap to meet the lowered
           MCL, even using state-of-the-art treatment, and so
           samples should be averaged; and
        0  that, while the effectiveness of specific treatment
           procedures varies in not-yet-well-understood ways when
           actually used  in the field, corrosion control  is ulti-
           mately feasible with current state-of-the-art  methods.
     Jacobson, using data from EPA Region I and the Massachusetts
Water Resources Authority, calculated  the benefits of additional
2-stage treatment for Boston's water:  further raising the pH  (to
reduce the acidity of the water)  and  installing several pumping
stations  to  maintain  a consistent concentration of  sodium hydroxide
throughout the system.
     Jacobson used the same categories of monetized health benefits*
as those  described  in this  EPA analysis,  except  that  he  did
not include  the  estimates of  cognitive damage associated  with
decreased future earnings.  His  estimates  of  materials  benefits
rely only upon  the  Kennedy  Engineers (1978)  study and information
 in the American Water Works Association  Corrosion Manual (AWWA-DVGW,
 1985).
 * For blood-pressure-related estimates, however, he used the non-
   site-adjusted coefficients from the NHANES II contained in
   Pirkle et al., 1985,

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                              1-27





     His results, summarized in pages 36-39 of his study, indicate



incremental costs of $700,000 per year (using sample year 1988) and



incremental annual benefits of $7.9 million (including estimated



health benefits of $6.9 million and materials benefits of



$950,000; based upon sample year 1988).  This yields estimated



net annual benefits of $7.2 million and a benefit to cost ratio



of 11:1 (compared to the estimate of 4:1 in this analysis).



     It is, however, unclear whether or how these results can be



extrapolated to other U.S. water systems and cities, and



therefore, to this proposed rule.

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                            CHAPTER II

               OCCURRENCE OF LEAD IN DRINKING WATER


     Lead can contaminate drinking water through several pathways.

It can result from naturally present lead in the source water, it

can result from contamination of the water supply, or it can

result as a by-product of corrosive water.*  In the last case, the

sources of the lead are the pipes, plumbing fixtures, flux and

solder of the distribution system and within private residences

or other buildings.  Most contamination of drinking water with

lead results from the corrosion of materials containing lead.

     Section A of this chapter discusses the sources and factors

affecting the contamination of drinking water by lead.**  Section B

of this chapter discusses the available data on the occurrence of

lead in community drinking water supplies.  Because lead occurs in

drinking water primarily as a corrosion by-product, contamination
*  Corrosion is the deterioration of a substance or its proper-
   ties due to a reaction with its environment.  In this paper,
   the "substance" that deteriorates is the pipe — whether made
   of metal, asbestos-cement, cement, or plastic — and the flux
   and solder joining the pipes, and the "environment" is water.
   That is, we are concerned with internal corrosion.  (Pipes and
   other water treatment equipment can also corrode externally.)

** Chapter V also contains a discussion of the relationship
   between corrosive water and lead in drinking water, but from
   the perspective of potential corrective action.

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                               II-2


levels are higher in tap water in homes* than in the water leaving

the water treatment plant or flowing through the water mains.

Section C contains EPA's estimates of exposure to lead in the

drinking water provided by community water systems in the

United States.

     The exposure estimate presented in this chapter serves as

the basis for calculating the benefits from a potential reduction

in exposure due to a lowering of the Maximum Contaminant Level

(MCL) for lead from the current 50 micrograms of lead per liter

of water (ug/1) to 20 ug/1.**


II.A.  Sources of Lead in Drinking Water

     The principal source of lead  in ambient surface water is

anthropogenic lead particulates from the atmosphere, which come

mostly from the combustion of leaded gasoline  (e.g., Laxen and

Harrison, 1977; Trefry et al., 1985) and, to a lesser extent, the

smelting of ores and the combustion of fossil  fuels.  Evidence

indicates that much of the lead in surface waters will end up in

sedimentary deposits  (Laxen  and Harrison, 1977) , and most of the
*   Lead contamination of drinking water  as a result of corrosion
    also occurs  in commercial buildings,  schools, etc.  There  is
    less information on  the  factors  that  determine  lead levels  in
    these buildings, however, than on  the use patterns and materials
    in private homes.  Therefore, this analysis  examines  only
    exposure  to  lead in  residential  circumstances.  Additional
    research  is  needed in other  areas  of  exposure,  including the
    work place  (factories, office buildings, etc.)  and in schools.

**  This is equivalent to and can be expressed as 0.020 milligrams
    per liter  (mg/1) , 0.020  micrograms per gram  (ug/g) , or 20  parts
    per billion  (ppb).

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                               II-3


lead dissolved in rain will precipitate and be filtered out by

the soil.  Lead from runoff or fallout will also precipitate and

be retained within the soil or sediments.

     The source of most lead in ground water is geochemical; that

is, the minerals contained in the rocks and soil through which the

ground water flows.  Concentrations of lead in ground water in the

United States are typically under 10 ug/1 (Levering, 1976) and,

generally, lead solubility is very low in ground water.

     The principal source of lead in drinking water is neither

naturally occurring lead in ground water nor anthropogenic lead in

surface water, however.  It is the materials of the water supply

and distribution systems and the plumbing in homes and other

buildings.  (See sources as diverse as Craun and McCabe, 1975;

[U.S.] National Academy of Sciences, 1977; EPA's Lead Technologies

and Costs Document, 1984; Kuch and Wagner, 1983; AWWA-DVGW Coopera-

tive Research Report,  1985; EPA's Lead Occurrence Document, 1985;

EPA's Air Quality Criteria Document for Lead, 1986; etc.).  The

highest concentrations of lead are found where pipes or solder

containing lead are used in combination with corrosive waters,

where water has been sitting for many hours, or where there is

newly-installed piping or repaired joints using flux or solder

containing lead.


II.A.I.  Variables Affecting Lead Levels in Drinking Water

     The lead used in service pipes* or as part of lead/tin solder

is relatively resistant to corrosion under simple laboratory
*  Service pipes connect the main pipes of the water distribution
   system to the plumbing contained within the home.

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                               II-4


conditions.  In addition, it can be protected from corrosion by a

thin layer of relatively insoluble film, composed of carbonate

compounds of lead or calcium, that forms on the surface of the

metal (Patterson and O'Brien, 1979; Schock and Gardels, 1983;

Lassovszky, 1984; etc.)-  Water, however, is a corrosive substance,

     In addition, the combination of copper piping with tin/lead

solder found in most residences can result in galvanic corrosion,*

which can yield lead levels much greater than expected from the

simple corrosion of the water alone.

     Other conditions typical in private homes exacerbate the

results of galvanic corrosion and can contribute to high lead

levels in home tap water.**  These include the facts that residen-

tial plumbing materials are often less corrosion resistant and

well-protected than those used in distribution systems (AWWA

Committee Report, 1984) , that water often remains overnight in

household pipes, and that some water used in private homes is

heated, greatly increasing its corrosive potential.


II.A.I.a.  Key Water Parameters Affecting the Solubility of Lead

     All water is corrosive to some degree.  However,  some quali-

ties of water make  it more corrosive for certain materials.  The

solubility of lead  (also called plumbosolvency) is complicated.
*  Galvanic corrosion results when  two metals, with different
   electrochemical potential, are in  the  same environment.

*  The maximum equilibrium  level  is determined by  the  specific
   qualities of  the water.  Because waters  in public drinking
   systems rarely reach equilibrium levels  (for purposes of
   corrosion) , non-equilibrium conditions are assumed  in the
   analysis presented in  this document.

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                               11-5


Probably the master control variable in the solubility of lead is

pH,* although it is closely interrelated with carbonate.**

Waters below pH 6.8 are very plumbosolvent, as can be waters with

pH above 10.2 (e.g., Moore, 1973; Schock, 1980; Sheiham and

Jackson, 1981; Murrell, 1985) , but pH does not have a strictly

linear relationship to lead levels in water (e.g., Patterson and

O'Brien, 1979; Pocock, 1980; Schock and Gardels, 1983) .  In

addition, at low or very high carbonate alkalinities,** lead is

soluble throughout the pH range of drinking water (e.g., Department

of the Environment, 1977? Pocock, 1980; Jackson and Sheiham,

1980; Schock, 1980; Sheiham and Jackson, 1981; Kirmeyer and

Logsdon, 1983; Schock and Gardels, 1983; Gregory and Jackson,

1984; AWWA-DVGW Report, 1985).  Soft watert is usually plumbosol-

vent, but several studies have shown that very hard water can

also be plumbosolvent (e.g., Department of the Environment, 1977;
*   The factors of water that inhibit or enhance corrosion are
    discussed in Chapter V, including measures of those para-
    meters.  In short, pH is a measure of the concentration of
    hydrogen ions (H+) in the water, which is important because
    H+ is one of the major substances that determines how much
    metal can be corroded electrochemically.

**  The carbonate content (measured indirectly by alkalinity
    and pH, and usually given in units of equivalent calcium
    carbonate, CaC03) relates mostly to the presence of dissolved
    bicarbonate and carbonate ions in the water and enables the
    formation of a relatively insoluble protective coating on the
    inside of the pipe, forming a barrier between the water and
    the materials of the plumbing system.

t   Water with low levels of calcium and magnesium ions, which
    can help form a protective coating on the inside of the pipe.
    Hardness is also expressed as the equivalent quantity of
    CaC03 (calcium carbonate).

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                               II-6






Thomas et al., 1981).  Other properties of the water, including



temperature (e.g., Mullen and Ritter, 1980; Britton and Richards,



1981); velocity; treatment with chlorination or chloramination*



(Treweek et al., 1985); presence of humic substances (Moore,



1973; Samuels and Meranger, 1984); chloride and nitrate levels



(Oliphant,  1982); and dissolved oxygen or other elements, may




also affect plumbosolvency.






II.A.l.b.  Lead Solder



     The use of lead/tin solder, in a tin to lead ratio of 50:50




or 60:40, is ubiquitous in U.S. residential plumbing at present



(e.g., Lead Industries Association, 1982; Chin and Karalekas, 1984;



AWWA-DVGW Report, 1985).  Lead solder is probably the greatest



single contributor to lead contamination of drinking water in



this country because of its widespread use and easy solubility.



Its easy solubility  is caused by the galvanic reaction between



the lead/tin solder  and the copper pipes that are used most



commonly in residential plumbing  (Anderson, 1984).  Many recent



studies have shown that solder containing lead, when used with



copper household plumbing, could easily raise lead levels above



50 ug/1, even when in contact with relatively non-corrosive



water or within a relatively short period of time  (e.g., Wong and



Berrang, 1976; Nielsen, 1976; Department of the Environment,




1977; Lyon and Lenihan, 1977; Lovell et al., 1978; Britton and



Richards, 1981; Sharrett et al., 1982a and b; Oliphant,  1982 and
*  Chemicals used in drinking water disinfection.

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                                II-7






1983; Samuels and Meranger, 1984; Birden et al., 1985; Treweek et



al., 1985).  Some of these and other investigations (e.g., Depart-



ment of the Environment, 1977) also found that lead solder alone



could produce lead contamination levels that were as high or



higher than those in wholly lead-plumbed houses.  Indeed, under



some conditions, because of the galvanic action they can be much



higher (Oliphant, 1982 and 1983; Murrell, 1985).  Data summarized



in the AWWA-DVGW Report (1985) , Table 4-19 and elsewhere, show



that even without new solder, the galvanic reaction in relatively



non-corrosive waters (pH 7.5-8.5, alkalinity > 100 mg/1 as CaC03)



can produce lead levels at the tap of 160-250 ug/1 upon overnight



standing.  Because both the solder and the copper piping must be



exposed, however, galvanic corrosion is usually a more serious



problem with new plumbing.



     Many studies have shown that the age of the lead solder is



among the most important variables affecting solubility.  For



example, Sharrett et al. (1982a) — studying Seattle, a city with



few lead pipes — found that the age of the house (a proxy measure



for the age of the solder and other plumbing materials) was the



dominant factor for predicting the concentration of lead in the



tap water.  In homes that were newer than five years old, with



copper pipes, the median lead concentration for standing water



was 31 ug/1 versus 4.4 ug/1 in older homes.  In homes built



within the previous 18 months, the median lead level was 74 ug/1.



     New solder will leach lead even in relatively non-corrosive



water — whether naturally less corrosive or treated (e.g., Nielsen,

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                               II-8





1976; Herrera et al., 1981) — and will continue to leach signifi-



cant amounts for up to five years  (Lovell et al., 1978, Sharrett



et al., 1982a; Oliphant, 1982 and 1983; Murrell, 1984; Lassovszky,



1985; Neff and Schock, 1985; etc.).  Murrell (1985)  found that



new solder could leach sufficient lead to contaminate standing



water to a degree hundreds of times higher than the current MCL;



this has been confirmed by data collected by the Philadelphia



water utility (1985) and elsewhere.  Oliphant  (1983) has also



shown that no matter how small the area of exposed solder, pro-



vided the contact time is long enough, the lead levels will always



exceed 100 ug/1 if the volume of  the sample is small.



     With new (exposed) solder, the duration of contact need not



be long to raise lead levels significantly.  Britton and Richards



(1981) and Lyon and Lenihan  (1977) have shown  that, with particu-



larly corrosive drinking water, lead levels in standing water in



systems with copper plumbing joined with lead  solder could rise



above 100 ug/1 within 40 minutes  of contact.   Oliphant  (1983) has



presented evidence that those conditions can produce lead levels



one to two orders-of-magnitude higher  than expected from equilib-



rium solubility calculations.



     Two other factors will  affect the rate of lead leaching from



lead-soldered joints:  the  surface area of the lead/tin solder  at



the joints  (which can often  relate to  the quality of the plumbing



and jointing work) and the  number  of joints per length of pipe



(e.g., Nielsen, 1975 and 1976; Lyon and Lenihan, 1977; Walker and



Oliphant, 1982b; Oliphant,  1983;  Birden et al., 1985; Lassovszky,

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                               II-9





1985; Murrell, 1985; Treweek et al., 1985).  It has also been



suggested that with pipes running vertically, the lead solder can



drip down the pipe, resulting in more exposed solder than in hori-



zontal pipes  (Arthur Perler, U.S. EPA, private communication).



     Lead solder in brass kitchen faucets can result in particu-



larly high concentrations of lead (Samuels and Meranger, 1984).



     Only one paper that we are aware of (Thompson and Sosnin,



1985) suggests that lead solder does not contribute significant



amounts of lead to water.  In that article, although the measure-



ments are presented as first-draw standing levels after a 12-hour



exposure period, the data shown are really for flushed (running)



samples (termed 'steady-state values').  The article was based on



a report (Battelle, 1982) that contains the actual data on lead



levels.  In that report, first-flush samples averaged above



50 ug/1 (Figures 22, and 23, and Table 50 of the Battelle report).



This is acknowledged in the narrative on page 33 of the report,



but discounted because the lead content decreases with time.



Therefore, the results of the Battelle study are consistent with



the rest of the literature.



     The easy plumbosolvency of lead solder has been known for



many years.  As a result, the Netherlands banned lead solder in



1977, Germany banned the use of lead solder about the same time",



and several states and localities in the United States have



banned it within the past few years.  The 1986 Amendments to the



Safe Drinking Water Act prohibit the use of materials containing



lead in public water systems, a prohibition that is enforceable



by the States after June 1988.

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                              11-10





II.A.I.e.  Lead Pipes



     Several characteristics of lead piping also influence lead



levels in drinking water (Poeoek, 1980; Britton and Richards,



1981; etc.).  The length of the lead pipe, in both the home and



the supply lines, can have a positive association with lead levels



Kuch and Wagner, 1983; Department of the Environment, 1977; Pocoek,



1980; Karalekas, 1984) as can the position of the pipe — it



appears that, even for the same length of pipe, water composition,



etc., lead piping contained wholly or partly within the house (as



opposed to lead service connections outside the house) correlates



with higher first-draw lead levels.  The ratio of the surface area



of lead exposed to the water volume contained is also important



(Ainsworth et al., 1977).  The age of the dwelling or the pipe



(Ainsworth et al., 1977) and the percentage of lead piping in



both the service mains and within the residence are significant



in determining lead levels, as well.   New lead pipes appear to



leach higher levels of, lead initially, with the rate decreasing



within a few days or weeks (Ainsworth et al., 1977).





II.A.l.d.  Other Potential Sources of Lead



     Lyon and Lenihan (1977) and others have found that the flux



used for soldering is an excellent electrolyte and can contribute



significant amounts of lead to drinking water.



     Some lead can also leach from copper pipes themselves (Herrera



et al., 1981).  Specifications for copper pipes usually limit



only copper and phosphorus, and copper used for non-drinking



water applications is permitted to contain some lead.  Copper



pipe manufacturers have indicated that copper tubing used for

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                               11-11

water can be made from  recycled copper products,  thus permitting
the  introduction of lead  impurities  (Herrera et al., 1981).
Although not common, lead  impurities can  also occur  in galvanized
pipe (e.g., Nielsen, 1975).
     Lead is also used  in  the  production  of brass and bronze.
Brass is a copper-zinc  alloy,,  which can contain up to 12 percent
lead, and bronze is a copper-tin alloy, which can contain up to
15 percent lead (U.S. EPA, 1982b).  While both are relatively
corrosion resistant and are not generally recognized as a source
of lead, several studies document lead leaching from brass or
bronze fixtures (Nielsen,  1975; Samuels and Meranger, 1984;
Neff 1984; Neff and Schock, 1985; Neff et al., 1987).
     Lead can also contaminate potable water when used in pipe
jointing compounds and  through its use for goosenecks, valves,
and gaskets in water treatment plants or distribution mains.
     At least one study (Herrera et al.,  1982) found that lead can
leach from tin-antimony solder "presumably com[ing] from impurities
in the solder."
     Early tests of plastic pipes showed that lead contamination
resulting from stabilizers used with polyvinyl chloride (PVC) pipes
could be high (studies summarized in National Academy of Sciences,
1982; volume 4, pages 64ff).  However, since then, the National
Sanitation Foundation has developed a standardized .testing pro-
cedure for plastic pipes.
     Additional analyses of the leaching of lead from these and
other sources is needed (AWWA-DVGW Report, 1985).

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                              11-12

II.A.I.e.  Other Factors Relating to Lead Contamination Levels
     The most important other variable affecting lead levels in
drinking water is the length of contact time between the water
and the plumbing materials.  High lead levels are found in water
from faucets that are seldom used or in the first drawn samples in
the morning after the water has sat overnight.  Usually, flushing
the faucet will significantly decrease the lead levels in the
water.  This is true for all waters, corrosive and less corrosive.
With very corrosive waters or new solder, the length of contact
time need not be great — as little as 40 minutes to an hour can
produce  lead levels above 100 ug/1 under certain conditions
(e.g., Lyon and Lenihan, 1977; Britton and Richards, 1980; Kuch
and Wagner, 1983; Oliphant,  1983).
    The  number of occupants  of the dwelling  is  inversely propor-
tional to lead levels, probably because  fewer occupants means  the
water will, on average,  remain in  the pipes  longer  (Department
of the Environment,  1977; Pocoek,  1980).
     Other  factors  that  can  affect lead  levels  in tap  water  are
pipe  length and  diameter,  and water  velocity (Bailey and Russell,
1981; Kuch  and Wagner,  1983).  No  matter what metal  the pipe is
made  of, the diameter  of the pipes is  inversely proportional to
lead contamination  levels  because  of the greater proportion of
water in contact with  the  lead-containing  surface (solder,  flux
or pipe) in pipes with smaller  diameters (Crank,  1975).  The
 length  of the metal pipe can correlate directly with the potential
 for  high lead  concentrations although not  consistently (Sharrett

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                              11-13

et al., 1982a; Kueh and Wagner, 1983).  Lead levels can also
increase with the turbulence and velocity of the water, and with
irregular flow patterns.

II.A.l.f.  Summary
     Because lead levels in tap water are a complicated function
of the specific qualities of the water, the particular materials
comprising the distribution and household plumbing, and the
length of time the water is in contact with the plumbing materials
as well as other factors, there is a high degree of within-house
and between-house variability in water lead levels (Sartor et
al., 1981; Bailey and Russell, 1981).  with even mildly aggressive
(corrosive) water, however, any amount of lead anywhere in the
distribution system or household will contribute some lead to the
drinking water.  Overall, there are four major risk factors:  the
the degree of corrosivity, the length of time in the pipe, the
total amount of lead in the plumbing materials, and the newness of
the plumbing.
     In general, lead levels in first-draw water can be several
times higher than in running water (e.g., Battelle, 1982).  With
aggressive waters and new solder,  however, first-draw samples can
easily be an order-of-magnitude or more greater than running
levels (cf. data in Karalekas et al., 1975;  Oliphant,  1983;
Maessen et al., 1985;  Murrell, 1985;  etc.).   Lead concentrations
in fully flushed samples typical of distribution system water,

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                              11-14


even under corrosive conditions and with new solder, are generally

below 50 ug/1 and are usually below 20 ug/1.*


II.A.2.  Prevalence of Lead Materials in Distribution Systems

     Lead has been used for plumbing materials since at least

Roman times.  It was considered a convenient and suitable

conveyance of water and was used extensively for water pipes

during the nineteenth and early twentieth centuries.

     The danger of lead contamination of drinking water was not

unknown, however.  In 1845, the Report of the Commissioners to

Examine the Sources from Which a Supply of Pure Water May Be

Obtained for the City of Boston concluded, "Considering the

deadly nature of lead poison, and the fact that so many natural

waters dissolve this metal, it is certainly [in] the cause of

safety to avoid, as far as possible, the use of lead pipe for

carrying water which is to be used for drinking."  Lead pipes

were outlawed in several German states in the second half of the

nineteenth century because of concern over health  (cited in AWWA-

DVGW Report, 1985; p. 223).  And a warning of potential danger

from lead pipes was given to the New England Water Works Associa-

tion in 1900 (Forbes), showing that the risk was known there, as

well.
*  This pattern of lead contamination also holds in Canada.  Data
   on lead contamination in raw, treated and distributed water
   from 70 municipalities across Canada show levels averaging
   1 ug/1  (Meranger et al., 1979).  On the other hand, a study of
   lead levels in waters that had sat overnight in home plumbing
   showed 20 percent of the samples exceeding 50 ug/1, with a
   mean level of 43 ug/1 (Maessen et al., 1985).

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                               11-15

      Despite these and other warnings,  in 1924 Donaldson reported
 that half of the 539 cities he surveyed in the early 1920s used
 lead or lead-lined service pipes.   He  found the greatest usage  of
 lead service lines in New England,  New  York,  the Midwest,  Texas,
 Oklahoma and Montana.
      Because lead is a relatively durable material,  many of the
 original lead lines  are still  in service (Patterson  and  O'Brien,
 1979).
      More recently,  Chin and Karalekas  (1984)  surveyed 153
 publ-ic  water systems  in 41  states,  Puerto Rico and the District
 of Columbia,  to  ascertain the  prevalence of  lead  materials  in
 distribution systems.   Their survey targeted  large systems, with
 91 of the 153 systems  surveyed serving populations over  100,000
 people.   (Nationally,  only  0.5 percent of  community water systems
 serve over 100,000 people.)  They found  that  almost three-quarters
 of the  systems had used  lead service lines or  connections  (most
 of the  remaining quarter  did not know if they had any lead or
 lead-lined services), and one city  (Chicago) still installed lead
 service  lines.*  In addition, almost two-thirds of the systems
had lead goosenecks in their plumbing (another 10 percent didn't
know if they had any) and about half of the systems reported
the use of solder or flux containing lead in the distribution
system.**
*   The installation of new lead pipes is now prohibited in
    Chicago.
**  The utilities may be referring to use in home plumbing or
    in service lines.

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                              11-16






     The use of lead/tin solder is ubiquitous in U.S. residential



plumbing at present.  Indeed, until 1986, most local plumbing and



construction codes recommended or even required the use of copper



pipe joined by lead/tin solder.  The 1986 Amendments to the Safe



Drinking Water Act banned the future use of materials containing



lead in public water systems or in residences connected to public



systems.  The ban became effective immediately (June 19, 1986),




but States have up to two years to enforce this provision.






II.B.  Data on the Occurrence of Lead in Drinking Water



     Under the provisions of the Safe Drinking Water Act, EPA



must ensure that public drinking water supplies are free of



contamination and that they comply with primary drinking water



regulations; this authority includes setting monitoring require-



ments to assess compliance.  Sections 1401(1)(D) and 1445(A)(1).



According to EPA regulations, monitoring for inorganic compounds,



including lead, must be conducted once per year for  systems whose



source  is surface water and once every three years for water-



supplies using ground water.  40 CFR  §141.23.  MCLs  are  defined  as



"the maximum permissible  level  of a contaminant in water which



is delivered to the free  flowing outlet  of the ultimate  user of  a



public  water system."  40 CFR  §141.l(a).   "Free flowing" has been



generally understood by the  States  and the water utilities to



mean a  "fully  flushed" sample.   In  addition, the procedures  for



laboratories  certified for  reporting  purposes  under  EPA's Laboratory



Certification  Program, administered by the Office  of Drinking Water,




specify that  the  sample be  taken after  running  the water for two

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                               11-17


 or  three  minutes  (U.S.  EPA,  1982c).  However, because  lead  is a

 corrosion by-product, these  procedures  decrease  the  likelihood of

 detecting lead contamination.  Therefore, the data collected for

 compliance with the Safe Drinking Water Act, as  administered

 currently by EPA, does  not adequately represent  exposure to lead

 in  U.S. drinking water.

     Several studies have investigated  the quality of  drinking

 water in  the United States,  including lead levels (e.g., the

 National  Inorganics and Radionuclides Survey, the National

 Organics  Monitoring Survey).   But these surveys have also not

 addressed the phenomenon of  most lead contamination of drinking

 water —  as a corrosion by-product.  These surveys have sampled

 lead levels in fully-flushed water typical of distribution water.

 Again, this sampling procedure minimizes the likelihood of  detec-

 ting the  contamination  of tap water by  lead.  Several other

 studies of national water quality have been conducted over the

 past two  decades (e.g., the  1969 and 1978 Community Water System

 Surveys,  the Rural Water Survey,  the First National Health and

 Nutrition Examination Survey), but the results from those surveys

have not been used by EPA in setting national standards.  (See,

 for instance,  U.S.  EPA,  1985; or 40 CFR Part 141, page 46969.)

     The estimate of occurrence,  therefore,  is based upon data

 collected and analyzed for EPA's  Office of Drinking Water in

 1979-81.  These data portray partly-flushed (30 seconds) kitchen

tap samples collected by the Culligan Water-Softening Company;*
*  The use of company names and the presentation of related data
   does not constitute endorsement of their services.

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                              11-18






James Patterson of the Illinois Institute of Technology analyzed




the data.  EPA believes that the Culligan tap samples are more



representative of consumed water than are the fully-flushed



samples taken in compliance with EPA's monitoring regulations.



In addition, these samples of partly-flushed, random daytime water



are more appropriately used with the water-lead-to-blood-lead



equation accepted by EPA than would be data on fully flushed water




or even a value integrating average consumption patterns.



     After the presentation of the Culligan data, this section



also includes a discussion of potential biases in the data, the



consistency of the findings with field and laboratory results,



and an alternative analysis of the potential contamination of



drinking water by lead  (to confirm the magnitude of the estimates).



     Finally, because homes with newly-installed plumbing contain-



ing lead solder or flux have a higher risk of elevated lead levels



than homes with older plumbing, this section also discusses




exposure to lead likely to occur in new housing.






II.B.I.  Patterson Study/Culligan Data on Tap Water



     In  1979-1980, EPA's Office of Drinking Water funded a study




by James Patterson using data  on residential water quality



 (Patterson, 1981).  The study,  "Corrosion in Water Distribution



Systems", analyzed 772  municipal water samples  collected by



Culligan Water Softening dealerships in  580  cities in  47 states.



The  samples were  collected  from May  to November 1978 at  the



consumers'  kitchen taps.  No samples were collected  from households




using home  water  softeners.

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                               11-19

      The  purpose  of  this  study was  to  evaluate  the  relationship
between different corrosion  indices  and  water quality variables
likely to influence  water corrosivity  against the observed  levels
of  the corrosion  by-products  iron, copper,  lead  and  zinc.   The
impetus for EPA1s commissioning of this  analysis was  probably
the  suggestion of the court  in a lawsuit brought by  the Environ-
mental Defense Fund  against  the Agency.  EDF v.  Costle, 578 F.2d
337,  349-50 (D.C.  Cir. 1978).   In addition  to containing data on
the  levels of these metals,  the analysis contained  information  on
calcium, magnesium,  sodium, pH, alkalinity, chloride,  conductivity,
sulfate,  and silica  levels in  each sample.  Calculations of
hardness  and corrosivity  indices (including Langelier, Ryznar,
Aggressive, Driving Force, and Larsons,  as  well as Dye's Momentary
Excess)  are also  presented.
     Water samples were collected by Culligan Dealership repre-
sentatives throughout the United States, after the kitchen tap
had been  flushed  for 30 seconds at a moderate flow rate, according
to a standardized sampling procedure.  All  samples were collected
in virgin plastic polypropylene bottles with plastic screw tops.
The metals analyses were conducted by the Illinois Institute of
Technology and the other analyses were done by the Culligan
laboratory in  Northbrook, Illinois.   Most samples were collected
between  10:00  a.m. and 8:00 p.m.
     For  lead  determinations, lithium nitrate was added to the
acidified sample  (although not until the samples were transferred
to glass  bottles)  and the flameless  graphite furnace atomic

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                              11-20





absorption procedure was employed.  The standard addition technique



was used for all lead determinations, to avoid certain common



interference problems.  Standard Methods (1971) were employed for



the analysis of all samples, except for the atomic absorption



procedures, where Perkin-Elmer  (1977) procedures were used.



     Analytical tests were conducted to evaluate potential testing



and analytical biases, both upward and downward.  To test for



upward bias (contamination that would increase apparent lead



levels), nitric acid was stored in the plastic sample bottles for



two weeks to draw out any lead  in the plastic bottle itself,



which could otherwise contaminate the sample.  The liquid was



then tested for lead presence,  and there was none.  Blank samples



(i.e., bottles  filled with lead-free distilled water) were also



used to check for upward bias.  After a period of standing  (two



weeks), the distilled water was tested  for  lead contamination;  it



remained lead-free.  These efforts showed that contamination of



the samples from the plastic bottle  itself  was unlikely.



     On the other hand, because no nitric acid was  used  to pre-



serve  the  samples until  the water  samples were  transferred  to



glass  vials,  there  was a possibility that some  lead  from  the



sample would  adsorb to the  plastic bottle;  this  would  bias  the



results downward  (i.e.,  lower  the measurable  lead  level).   Spiked



samples (i.e.,  solutions with  a known  amount  of  lead)  were  used



to test for this.   The results indicated  that,  on  average,  3  ug/1



of lead adsorbed onto  the  plastic  bottle;  therefore,  a slight



downward  bias was  present  in  the  results.

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                               11-21





      Calibration and  other  analytical  controls were also employed



 at several  points in  each batch  as part of  the laboratories'



 ongoing  quality assurance and  quality  control  efforts.   (Full



 documentation  is available  from  each lab.)



      These  data indicate that  16 percent of partly  flushed  water



 samples  could  exceed  an MCL of 20  ug/1 at the  kitchen tap,  and



 that  3 percent exceed  the current  MCL  of 50 ug/1.   Fifty-two



 percent  of  the samples contained 9 ug/1  or  less of  lead,  the



 maximum  was  10,000  ug/1.  The  occurrence of high lead levels was



 geographically widespread.   Samples with lead  levels greater than



 20  ug/1  were taken  in more  than  half of  the  states  in the country,



 and in every one  of EPA's ten  Regions.   The  distribution of lead



 levels in these  samples is  presented in  Table  II-l.





 II.B.I.a.  Consistency with  Other  Data




     The literature on contamination levels due to  lead leaching



 from plumbing materials shows great variations relating to the



 specific conditions being observed.



     The Culligan data, with 16 percent of  the samples exceeding



 20 ug/1, have a lower incidence rate of high lead concentrations



 than is commonly portrayed   in the literature on lead leaching



 rates and the potential for  lead  contamination in tap water.



This is reasonable because  that literature,  in general,  focuses



upon high risk   (i.e.,  very corrosive)  waters.

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                              11-22
TABLE II-l.  Distribution of Culligan Data (Patterson, 19B1)
                             Measured Lead Concentrations
                                        (ug/D	
                     < 10
          11-19
          20-49    > 50
Percent of samples
60
24
13

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                               11-23


     The Culligan  samples, on  the other  hand,  do  not  portray

particularly corrosive waters.   in  these  samples,  the median  pH

is  7.2  (mean, 6.8), median alkalinity  is  106 mg/1  as  CaC03  (mean,

144 mg/1) , and median hardness  is 145  mg/1 as  CaCC>3  (mean,  203

mg/1).  These are  considered to  be  relatively  "non-corrosive"

waters.  Comparing the hardness  of  the water in these tap samples,

for instance, with the U.S. Geological Survey  estimates of  the

extent of soft water in the United  States  (Durfor  and Becker,

1964a and 1964b) or the data in  Millette et al. (1980),* these

samples represent water that is  much harder than  the  average  in

the country.  The  average Langelier Saturation Index** for  the

Culligan samples is -0.4, which  is  fairly stable.t it is logical

that less corrosive waters would contain a lower  incidence  of

corrosion by-products than do studies  of more corrosive water.tt
*   Both of these studies are discussed more extensively below in
    Section B.l.C. and in Chapter v.

**  One index used to estimate a water's potential corrosivity,
    discussed more fully in Chapter v.

t   A "stable" water is one where a film of CaC03 should be exact-
    ly at equilibrium, i.e., it neither dissolves nor deposits and
    grows.

tt  While it is hard to generalize about these studies, typical
    results under corrosive conditions show from perhaps 50-100
    percent of the samples exceeding 50^ ug/1 (e.g., Lyon and
    Lenihan, 1977; Department of the Environment, 1977; Britton
    and Richards, 1980; Oliphant, 1983) to 15-50 percent exceeding
    50 ug/1 (e.g., Karalekas et al., 1977; Karalekas et al., 1978;
    Seattle Water Metals Survey, 1978; Craun and McCabe, 1975).
    By comparison, the Culligan estimate (16 percent >20 ug/1)  is
    low.

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                              11-24
     The Culligan data portray higher levels of lead contamination,

however, than do either. EPA1 s data on compliance with the Safe

Drinking Water Act or most of the studies that have investigated

the quality of distributed drinking water in the United States,

including lead levels.  These surveys and EPA1s monitoring require-

ments have measured lead levels in water more typical of the

distribution system and most of the results indicate low levels

of lead contamination.*  Lead contamination, however, occurs

primarily in tap water and  in water that has been in contact

(standing) with pipes for some length of time.  Therefore, the

somewhat higher lead levels in the partially flushed, random

daytime tap samples that make up the Culligan samples confirm  the

findings from experimental  and field studies of lead leaching

rates and patterns.

     Perhaps the clearest indication of  the consistency of the

Culligan samples with other data on lead contamination of drinking

water is a comparison with  the preliminary  results  of EPA's  "Lead

Solder  Aging Study", presented in  U.S. EPA  (1987).  The lead

levels  in the partially  flushed  Culligan samples  are similar  to

those in housing over two years  old with median pH  (i.e., 7.0-7.4)

or  in waters with  high pH  (i.e.,  > 8.0).  The data  from  the  Lead

Solder  Study  are presented  in  Tables  II-3 and  II-4, below.
 *   For  comparison,  the National inorganics and  Radionuclides
    Survey,  recently conducted by EPA,  shows only about 1.5 per-
    cent of  ground-water-supplied public systems have lead  levels
    over 20  ug/1 in  fully flushed water.

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                               11-25


      The Culligan data serve as the basis for this analysis

 because, of the available data, EPA believes that they are more

 representative of the water consumed in this country than are the

 fully-flushed  samples taken in compliance with EPA's monitoring

 regulations.   People  drink the water from the taps in their homes

 after  it has been sitting for  unknown periods of  time.   While

 some  people may run their water before using it for  cooking or

 drinking, probably many  people (especially children)  do not.

 These  data  portray neither an  upper  bound for exposure  (which

 would  result from analyses of  first-flush samples) nor  a lower

 bound  (which would come  from an analysis  of fully-flushed distri-

 bution water);  they more closely portray  the bulk  of the water

 that  is  consumed  (e.g.,  Bailey and Russell,  1981).   Finally,  when

 controlling for other  environmental  sources  of  lead  exposure,

 studies  of  the  relationship between  blood lead  levels and water

 lead have also  found  a better  fit with  lead  levels in standing

 water  than  with fully-flushed  samples  (e.g.,  Worth et al.,  1981;

 Bailey and  Russell, 1981;  Pocock et  al.,  1983).*


 II.B.l.b.  Potential Biases in  the Data

     In determining whether it  is reasonable  to generalize  from a

 subset,  it  is important  to determine any  potential biases  in  the

data and, if found, to assess the likely  effect upon the  results.

Some potential biases   (for example, potential analytical  and
*  This issue is presented more fully in the section below on
   uncertainties, within the discussion of the relationship
   between blood lead levels and levels of lead in drinking water

-------
                              11-26

testing biases) as well as the consistency of the findings with
the literature on water quality and lead leaching rates were dis-
cussed in previous sections.  Others, for instance, the inclusion
of new housing within the data, are discussed below.  In this
section, we address the issues of potential selection bias,
geographic representation, and the implications of the relative
hardness of the samples.
     Because these samples were collected by a water treatment
company, a self-selection bias is possible; i.e., it is conceiv-
able that they represent water that is  'dirtier1 than average.
However, Culligan is not a general water treatment company and
does not test  for contamination by inorganic  (e.g., lead) or
organic  (e.g., pesticides) substances.  EPA and  the Illinois
Institute of Technology arranged  for  and conducted  the analyses
of metal contamination  in these samples.  Homeowners who had
general water  problems or who  had  reason to suspect that their
water  was contaminated would be unlikely to call Culligan  for
water  testing  or  treatment.  If they  did call  and  outline  such a
problem, the Culligan  representative  would have  either suggested
that  they contact another lab  in  the  area or  informed  them  that
Culligan would charge  extra  to arrange  for such  analyses.   There-
fore,  it is unlikely that there would be selection bias  resulting
in  higher  lead contamination levels.
      On the other hand,  a different  selection bias is  likely  and
did,  in fact,  occur.   Not  surprisingly, because  the samples were
taken by a water  softening  company,  overall  hardness  results  from

-------
                               11-27


 the Culligan/patterson data were higher than other data on water

 hardness in the country.*   For comparison,  only about 10 percent

 of the  Culligan samples contained soft water (i.e., < 60 mg/1

 as CaC03)  while in  the U.S. Geological Survey (Durfor and Becker,

 1964a and  b) ,** about  one-third  of the country had soft water.

 National patterns portrayed in the U.S. Geological Survey held  in

 this survey:  the Northeast  and Southeast had the  softest water,

 with the Midwest averaging  almost three times harder  water.   The

 Northwest  also  had  relatively  soft water.

     The highest lead  levels in  this data set were in the Midwest,

 which also  had  the  hardest  water.   The  combination of high, hardness

 and  high lead levels is somewhat  surprising;  usually  lead (as a

 corrosion by-product)  occurs more  frequently in softer  water.

 Schock  (1980 and 1981)  and  Schock  and  Gardels  (1983)  have shown,

 however, that at a  pH  of 8-8.5, soft water.(i.e.,  30  rag/1 as  CaG03)

may  be  less corrosive  to both  lead  and  copper  than can  be hard

 water (i.e., >  150 mg/1).   These  results confirm Patterson's

 findings (1981)   and the consensus  of the technical  literature:

Many inter-related  factors  affect  a water's corrosivity  and no

 single corrosivity  index adequately measures  the actual  corrosion

potential of a  specific water;  therefore, no single index  is a good

predictor of corrosion by-products, including lead.
    The range in hardness in the Culligan data is extreme:  from 2
    to 975 mg/1 as CaC03, with median 145 and mean 203.  Generally,
    levels over 240 mg/1 are quite uncommon.

**  The USGS data is discussed more fully in Chapter V.

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                              11-28

     But while no single measure of water quality is a good
predictor of the actual corrosion potential of a specific water,
the weight of the literature does show that softer water tends to
be more corrosive than harder water.  Therefore, this selection
bias may introduce some downward bias to the estimates; i.e.,
the concentrations of lead in the Culligan data may be somewhat
low relative to the actual levels in the country as a whole.
     Because the people who call Culligan can afford to pay for
those services, another potential self-selection bias is that
the population represented by these data is wealthier (and possibly
more sensitive to health and environmental issuses) and contains
a greater proportion of single-family and owner-occupied housing
than is  typical in the U.S. population.  It is  unclear what
effect this could have on the estimates.  A brief discussion of
possible contamination patterns  in multi-family housing, particu-
larly high-rise buildings, is included  in the section on uncer-
tainties, below.
     A question arises as to whether  the samples  are geographi-
cally representative of  the United  States.  The percentage of
samples  collected  from each state  closely reflects  the popula-
tion distribution  across  the United  States, with  a  few exceptions.
As  a proportion of percentage-of-samples to percentage-of-U.S.-
population,  the most  significant differences  are  the  states of
Alabama, Arkansas, North  Carolina  and Washington,  where  the dif-
 ference  varies by about  an  order of magnitude.   For the  state  of
Wyoming, the difference  is  a  factor of  5.   These  states  are

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                               11-29


relatively small and combined, contain only about 7 percent of the

U.S. population.  This could be expected because the smaller the

size of the observation, the larger the relative effect.  The

anticipated effect on the estimate is low.  For an impact upon

the final estimates, the most  significant differences are the

states of California, Colorado and Illinois, where the absolute

difference between the percentage of samples and percentage of

population differs by more than 5 percent of the total.  On a

regional basis, however, the distribution of samples closely

paralleled the population distribution.  The most significant

exception here is the Midwest; the percentage of samples (42

percent) was much larger than  the population (26 percent, 1980

Census).  Table II-2 presents  the distribution of samples by

state, and by region of the country.

     We conducted chi-square tests* of the distributions to

determine how closely related  they were.  The results were

inconclusive, however, because whether the results were significant

depended upon how finely subset the data were,  that is, how many

divisions (and, therefore, how many degrees of freedom)  for the

data were used.  The possibilities included 50  subsets (i.e.,  by

state, with 49 degrees of freedom), 10 (i.e., by EPA Region, with

9 degrees of freedom), 5 (i.e., using Patterson's groupings, with

4 degrees of freedom), or simply for the nation as a whole.
*  The chi-square statistic, represented by the Greek letter x
   raised to the 2nd power, is a measure of how much, propor-
   tionally, the frequencies in the observations differ from the
   frequencies you would "expect" if there were absolutely no
   relationship between the variables (Matlack, 1980).

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                              11-30
TABLE II-2,
Municipal Water Samples and Population Percentages
from Culligan/Patterson Study (Patterson, 1981)
State
Northeast States
CT
MA
ME
NH
NJ
NY
PA
RI
VT
Total
Southeast States
DE
FL
GA
MD
NC
SC
VA
WV
Total
Midwest States
IA
IN
IL
KS
MI
MN
MO
ND
NE
OH
SD
WI
% Population*

1.4
2.5
0.4
0.4
3.3
7.8
5.3_
0.4
0.2
22%

0.3
4.3
2.4
1.9
2.6
1.4
2.4
0.9
16%

1.3
2.4
5.1
1.0
4.1
1.8
2.2
0.3
0.7
4.8
0.3
2.1
% Samples

0.63
2.4
0
0.38
5.2
5.3
3.9
0.50
0.25
19%

0.25
2.9
1.8
1.3
0.25
0.63
2.6
2.4
13%

3.7
6.2
12.4
1.9
2.0
4.2
2.3
0.38
1.3
4.6
0.76
2.0
   Total
                  26%
                                                        42%
* U.S. Bureau of  Census,  1980.
  data were  used.
                    In  the  Patterson study,  1978  Census

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                              11-31
TABLE II-2.  (Continued)
State
% Population*
% Samples
Southcentral States
AL
AR
KY
LA
MS
OK
TN
TX
Total
Western States
AZ
CA
CO
ID
MT
NM
NV
OR
UT
WA
WY
Total

1.7
1.0
1.6
1.9
1.1
1.3
2.0
6.3
17%

1.2
10.5
1.3
0.4
0.3
0.6
0.4
1.2
0.6
1.8
0.2
19%

0.25
0
1.0
1.3
0.63
0.88
1.8
5.2
11%

2.0
2.3
6.3
0.51
0.88
0.88
0.51
1.3
0.25
0.13
1.0
16%
* Bureau of Census, 1980

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                              11-32


     To check whether the slight skewing of number-of-samples

compared to population-by-state affected the estimates, we weighted

the results by state population and compared that analysis with

the results of the national analysis (which assumed that the data

are geographically representative of the nation).  The results

differed by less than one-half of one percent.  We concluded that

the slight variation in geographic distribution does not signifi-

cantly affect the estimates.


II.B.I.e.  Alternative Analysis of Potential Exposure
           to Lead in Drinking Water

     Several bodies of literature are available for an alternative

analysis of potential exposure to confirm the magnitude of the

results from the Culligan data.  These include studies of the

extent of highly corrosive water in the United States and experi-

mental and field analyses of lead contamination.

     Two major studies have focused on assessing the extent of

highly corrosive water in the United States.*  They are the U.S.

Geological Surveys (USGS) conducted in the early 1960s (published

in Durfor and Becker, 1964a and 1964b) and the First Health and

Nutrition Examination Survey (HANES I), conducted by the National

Center for Health Statistics in 1974 and 1975.**  The results of
*   This information is presented more fully in Chapter V,
    section B.I.

**  The data from the Midwest Research Institute  (1979) and from
    Millette et al. (1980) on the extent of corrosive water in the
    country contain profiles that are quite similar to the USGS
    and the HANES I.  They are not included in this discussion,
    however, because this analysis addresses estimates of the
    extent of specifically soft water, not water  that is corrosive
    for other reasons.  Chapter V discusses these two studies as
    well.

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                              11-33


these studies can be combined with analyses of lead leaching

rates and the variables affecting plumbosolvency for comparison

with the findings from the Culligan data.

     The USGS data showed that 17 states had very soft water

(under 60 mg/1 as CaC03); using 1980 Census data, the combined

populations of those states is 67.7 million people.  The results

of the HANES I (as published in Greathouse and Osborne, 1980)

show a very similar picture:  about one-third of the country has

very soft water (under 60 mg/1 as CaC03).  Given a total current

(1985) national population of a little over 240 million/ about

80 million people receive very soft water.

     Numerous studies of plumbosolvency conducted in the United

States and in Great Britain have shown that soft, acidic waters

are most corrosive and have the highest lead contamination levels

(e.g., Craun and McCabe, 1975; Nielsen, 1976; Hoyt et al., 1979;

Patterson and O'Brien, 1979,; U.S. EPA, 1982b; Sheiham and Jackson,

1981; Worth et al., 1981).  There is some discussion as to whether

pH or carbonate content is the most important variable, and many

studies show that the relationship between pH or carbonate and

lead levels may be neither simple or linear.  In general, the

lower either value is, the more vulnerable the water to high lead

contamination.*

     Both laboratory and field experiments demonstrate this.

For instance,  data from Karalekas et al.  (1977) on two cities
*  Because neither the relationship between pH nor carbonate and
   lead is linear, this is not strictly true at all pH or carbonate
   levels.  Kuch and Wagner (1983) and Schock and Gardels (1983)
   among others have developed multi-dimensional models of lead
   solubility.

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                              11-34


(Bridgeport, Connecticut, and New Bedford, Massachusetts) with

similar pH levels  (7.1 and 7.3, respectively) but different

hardness and alkalinity  (48 and 18 mg/1 vs. 12 and 24 mg/1,

respectively) indicated that even with moderate pH the softer

water could contain six to eight times higher lead contamination

levels.  Schock and Gardels (1983), investigating water with high

pH (> 8.6) but low carbonate content, present average lead concen-

trations of 67-134 ug/1 in first draw water.  Other results

typical of this literature are the field data presented in the

Seattle Water Metals Survey (1978) and the laboratory data in

Sheiham and Jackson (1981).  In the former, highly corrosive

waters produced mean lead levels of almost 30 ug/1 (from lead

solder alone; there were no lead pipes) and in the latter, mean

lead levels were over 100 ug/1 with a mixture of lead and non-lead

pipes (some old, some new) and lead solder.  In sum, most studies

show that first flush samples from soft, corrosive water (i.e.,

hardness under 60 mg/1 as CaC03) often result in lead contamination

levels exceeding 50 ug/1* even in housing that is not new.  (New

housing is at particular risk of high lead levels.  This is

discussed in the next section.)

     Not everyone who receives very soft water, however, is at

equal risk of high lead exposure.  Some water systems with very

corrosive waters (Boston and Seattle, for instance) treat their

water to reduce its aggressiveness; their risk is lower.  A small

proportion of water utilities have lead in source water, as well
*  Because EPA's standard for lead is 50 ug/1, most studies have
   used that as the cut-off.

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                              11-35



as a corrosion by-product; their risk is higher.  Some localities


have few lead pipes and connections (and hence, have a smaller

likelihood of high lead contamination), while others have many.


Some localities have begun already to ban the use of materials


containing lead in public water supplies and in residences

connected to them.  In addition, plastic pipes are beginning to


be used in some residential plumbing,  even for bringing in potable

water,* replacing the metal pipes that are more likely to leach


lead.  Finally, at least one city (Akron, Ohio) has instituted an

active program to replace its lead service connections.

     To account for these variables and for the idiosyncracies of


specific waters, we assumed conservatively that with very soft

waters (i.e., hardness under 60 mg/1 as CaC03), half of first-

flush samples could exceed 20 ug/1, and that 10 percent of them

could exceed 50 ug/1.


     Combining information, then, on 1) the extent of very corrosive


water in the country (about one-third of the population receives

very soft water) and 2) studies of potential lead contamination

with very soft water (almost all have levels > 20 ug/1 in first-


flush samples and many also had levels > 20 ug/1 in random daytime


samples) but 3) mitigated to include some factors likely to decrease


exposure* (e.g., some cities have already begun corrosion control


treatment) yields the following calculation:
*  Plastic pipes are used more commonly for waste water than
   for intake.

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                              11-36
     1/3 of country x 50% occurrence of Pb>20 ug/1 =
          17% of population exposed to water >20 ug/1
     Therefore, this alternative estimate of potential exposure

to lead contamination of drinking water in non-new housing yields

results that are quite close to those of the Culligan data analyzed

by Patterson (1981), where 16 percent of the samples were greater

than 20 ug/1.  The results are most sensitive to the estimate of

lead levels > 20 ug/1.  (For comparison, assuming 25% occurrence

yields a national estimate of 8% and assuming 75% occurrence

yields a national estimate of 25% of the U.S. population exposed

to water > 20 ug/1.)

     There is additional anecdotal evidence that also supports

the patterns and extent of lead contamination presented here.

A CBS-affiliated television station in Cleveland, Ohio (Channel

8) conducted a small survey of lead levels in first-flush tap

water in early 1987.  They found 13 percent of the samples exceeded

20 ug/1, with a home occupied for only three months having lead

levels of >_ 100 ug/1.  Second, a water utility in Colorado (Little

Thompson Water District) conducted a limited survey of lead

contamination within customers' residences.  This survey was

conducted in conjunction with the Colorado Department of Health

and was accomplished concurrently with sampling programs in the

cities of Denver, Colorado Springs, and Fort Collins (Colorado).

The results from Little Thompson showed one-third of the residences

sampled exceeded 20 ug/1 — results they indicated "were comparable
*  Some factors, for instance, many lead pipes or lead contamination
   of distribution water, can increase exposure estimates, also.

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                              11-37



to the results of the aforementioned cities."  The highest reading

(> 400 ug/1) was in a riot-yet-occupied house.  Third, concern

about potential lead contamination of drinking water in Washington,

D.C. in late 1986 and early 1987 resulted in about 1,000 water

samples being taken there.  Newspaper reports (Washington Post)

and numerous press releases from the D.C. Department of Public

Health reported that between 13 and 25 percent of the water

samples exceeded 20 ug/1, and that the results indicated "that as

many as 56,000 houses may have problems with lead contamination,"


resulting from the common use of long lead service connections in

many parts of the city.  In addition, data collected by KYW-TV

in Philadelphia (an NBS-affiliate) in February 1987, by EPA's

Region IX (San Francisco) in Spring 1987, by the Nassau County (New

York) Department of Health in 1987, and jointly by the New Jersey

Department of Environmental Protection and the U.S. Geological

Survey (presented by J. L. Barringer at the American Geophysical

Union Spring 1987 meeting) show widespread lead contamination

following predictable patterns:  contamination levels are high

with new plumbing or corrosive waters, contamination is minimal

with non-corrosive waters and older plumbing.

     Finally, data available from WaterTest Corporation,* a


private water testing laboratory in Manchester,  New Hampshire, on

over 2,500 samples taken in January-March, 1987,  show that average

first-flush samples exceeded 20 ug/1 in 15 states plus the District

of Columbia.  This shows that the occurrence of lead levels

exceeding 20 ug/1 is widespread in this country but it was not
*  The use of company names and the presentation of related data
   does not constitute endorsement of their services.

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                              11-38






possible to determine the age of the housing from which the




samples came.



     This alternative analysis of potential lead contamination of



tap water was based upon assumptions about leaching rates in soft




water  (< 60 mg/1 as CaCC>3), but this is not the only factor that



makes water corrosive.  Many other parameters, including pH,




alkalinity, temperature, etc., contribute to corrosivity.



     People who receive water that is only moderately soft  (i.e.,



hardness between 60 and 90 mg/1 as CaC03) as well as those whose



45ter is not soft but has a low pH or has other risk factors




associated with aggressiveness (e.g., high levels of chlorine,



dissolved oxygen, chlorides, sulfates, etc.) also run a somewhat



elevated risk of exposure to high lead levels in drinking water.



However, the data on these circumstances are too sparce to use in



estimating populations at risk of high lead levels.






II.B.2.  Lead Contamination in New Housing



     As was discussed briefly in section A above, many studies




have shown that newly-installed lead solder (or pipes) can leach



high amounts of lead in a short amount of time.  Indeed, in studies



such as Sharrett et al. (1982a), the age of the house (a proxy



measure of the age of the plumbing) was the variable most closely



related to the lead concentration in the house water.  Table II-3



presents some field data on lead levels in new housing.  As can



be seen, the highest lead contamination levels occur with the new-



est solder (i.e., during the first 24 months following installation



those levels decline and generally are not elevated beyond five




years  (cf also, Sharrett et al., 1982a; Lassovszky, 1984; etc.).

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                                     11-39
TABLE II-3   Lead Contamination Levels in Tap Water by Age of Plumbing  (Field Studies)


Study
Sharrett
et al.
(1982a)
Nassau
County (1985)


Philadelphia
(1985)



EPA (1987)
preliminary
results

















Age of
Housing
<18 months
<5 years
>5 years
unoccupied
<2 years
2-10 years
>10 years
<2 years

>2 years

>4.5 years
<2 years


<2 years

<2 years

2-5 years

2-5 years

2-5 years

>5 years

>5 years

>5 years

Mean Pb
Level
(ug/1)
74
31
4.4
2,690
540
60
10
90
5000
60
500
<25
NG
NG

NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
% of
Samples
>2jO ug/1
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
NG
93%
51%

83%
5%
72%
0%
84%
19%
28%
7%
18%
4%
51%
4%
14%
0%
13%
3%


Cond i t ions/Notes
(Median standing levels
(No lead pipes
(
(Average, first flush
(
(
(
Flushed
First-flush
Flushed
First- flush
NG
First draw (pH <6.4)
Flushed, 2 minutes (pH <6

First draw (pH 7.0-7.4)
Flushed, 2 minutes (pH 7.
First draw (pH >8.0)
Flushed, 2 minutes (pH >8
First draw (pH <6.4)
Flushed, 2 minutes (pH <6
First draw (pH 7.0-7.4)
Flushed, 2 minutes (pH 7.
First draw (pH >8.0)
Flushed, 2 minutes (pH >8
First draw (pH <6.4)
Flushed, 2 minutes (pH <6
First draw (pH 7.0-7.4)
Flushed, 2 minutes (pH 7.
First draw (pH >8.0)
Flushed, 2 minutes (pH >8
















-4)


0-7

.0)

.4)

0-7

.0)

.4)

0-7

.0)



















.4)





.4)





.4)


KEY:   Pb = Lead
NG = Not given

-------
                              11-40





     Oliphant (1982 and 1983), studying the galvanic action



between lead solder and copper pipes, concluded that with any



amount of new (exposed) solder-alone (i.e., without lead pipes)



and sufficient time, lead levels will always eventually exceed



100 ug/1 if the volume of the sample is small.  The parameters of



the water (including pH and total carbonate) are irrelevant to



the prediction.  His analysis also showed that this galvanic



action can produce lead contamination levels 100-1,000 times



higher than equilibrium models would predict for the water itself.



Over time, however, protective passivation films usually build up



in the plumbing and such galvanic couples can stabilize eventually



at between 10 and 50 percent of the highest (initial) leaching



rates (Oliphant, 1983) or even lower (Lyon and Lenihan, 1977).



With copper pipes and new solder, flushed water samples can



exceed the current MCL (Philadelphia, 1985; Nassau, 1985; Kuch



and Wagner, 1983), although this is not common; the length of new



plumbing is probably a significant factor here.



     While new housing containing lead solder clearly represents



a significant risk of extremely high lead levels in drinking



water, the possibility existed that this risk was  included in the



samples collected by Culligan.  We evaluated this  in two ways.



First, we compared the incidence rate in the Culligan data (16



percent of the samples exceeded 20 ug/1) against the rates pre-



sented in studies of new plumbing (about 100 percent > 20 ug/1).



The literature on the leaching potential of new plumbing shows



much higher contamination levels than is evident in the Culligan



kitchen tap samples.  Therefore, the data indicate that it is



unlikely that these samples included new housing.  Second, we

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                               11-41






contacted Culligan dealerships in eight different areas, including




both areas of recent rapid growth and areas with relatively stable



growth patterns.  In each office, we asked the representative with




the longest sales record to describe the average Culligan customer



on a public water supply and to estimate how many customers on



public water supplies lived in new homes.  The representatives




contacted had served many thousands of customers and all described



their customers as generally calling Culligan with long-standing



problems; for residences connected to community water systems,



new problems and problems in new homes were perceived as going



first to the local public water utility.



     Inhabitants of new housing (i.e., built within the past




two years), therefore, represent a separate group at risk of




receiving water that exceeds 20 ug/1.  Because this population



is not represented in the samples of partially flushed kitchen




tap water, they must be added to the estimate of exposure.






II.C.  Estimated Exposure to Lead in U.S. Tap Water



     The estimate of exposure to lead levels in U.S. drinking




water _>. 20 ug/1 has several components:  1) the general risk of



high lead levels due to the corrosivity of all water and the con-



tact time between tap water and any materials containing lead, 2)




the specific risk to inhabitants of new homes (built within the



past two years), and 3) many assumptions, including the generaliz-




ability of the findings,  the distribution of the at-risk popula-



tions,  the relationship between lead levels in water and human



blood-lead levels,  compliance with a new regulation, and other



issues.

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                              11-42


     The first part of this section describes some of the many

uncertainties and assumptions included in this analysis.  The

second part presents estimates of potential exposure to tap water

containing 20 ug/1 of lead or greater.


II.C.I.  Uncertainties and Assumptions in the Analysis

     It is important to note some of the assumptions and uncer-

tainties that are both inherent and explicit in this analysis.


Assumption;  Total compliance.  This analysis assumes that, should

the MCL be reduced, all community water systems will comply with

the new standard by whatever means are necessary for that par-

ticular system.  In reality, if some systems do not comply, both

the costs and the benefits will be overestimated proportionately;

the benefit to cost ratio will remain the same because both are

functions of the number of people affected.

     No more than borderline compliance with the new standard is

assumed, however.  That is, if the MCL is 20 ug/1, we assume that

any systems currently exceeding that level will take measures

to reduce their water to that level.  If some systems act to reduce

lead levels further, both the costs and the benefits will be

higher? it is unclear what the ratio between the costs and benefits

would be for the incremental reduction.*
*  The case study of Boston (Jacobson, 1986), summarized in Chapter
   I and appended to this document, indicates that in particular
   circumstances, the benefit to cost ratio may be quite high —
   11:1 in that case.  It is unclear, however, whether or how
   Jacobson's results can be extrapolated to other U.S. water
   systems and cities and, therefore, to this proposed rule.

   It is unlikely, though, that there is any reasonable and
   practical scenario in which a water system would institute
   corrosion control measures where the incremental costs exceed
   the incremental benefits.  At a minimum, therefore, these
   costs and benefits should be assumed to be equal.

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                               11-43

 Assumption;  Treatment can generally reduce lead levels to 20 ug/1.
 In general, the data on corrosion control treatment show signi-
 ficant reductions in lead levels (e.g., Karalekas et al., 1977,
 1978, 1983; Herrera et al.,  1983).   However, efforts have generally
 focused upon reducing lead contamination to levels below the
 current MCL of 50 ug/1.  There is very little data on reducing
 lead levels below that.  Some preliminary data is available
 from EPA's "Lead Solder Aging Project."  These results, shown as
 Table II-4, indicate that simply raising pH alone greatly reduces
 the  occurrence of samples exceeding  20 ug/1.
      Field data from Patterson and O'Brien (1979) ,  Britton  and
 Richards  (1981)  and  others show  that adjusting the  alkalinity
 of the  water  also significantly  affects plumbosolvency.   Other
 studies  (e.g.,  Schock  and  Gardels, 1983)  adjusted  the level  of
 dissolved  inorganic  carbonate (DIG)  as  opposed to alkalinity,
 because DIG is  independent of pH  while  alkalinity is not.   These
 studies found  that increasing DIG could  slow  lead leaching  rates.
 Some  laboratory,  experimental, and theoretical  analyses have
 addressed  the effect of  simultaneously  altering several water
 parameters  (e.g., pH, alkalinity, inorganic carbonate, etc.) on
 plumbosolvency  (e.g., Schock,  1980; Jackson and Sheiham, 1980;
 Schock and Gardels, 1983; Sheiham and Jackson, 1981; Kuch and
Wagner, 1983).
     However, no treatment has yet been shown to be completely
successful in preventing all contamination of drinking water by
lead.  in particular, new (exposed)  plumbing containing lead

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                                     11-44
TABLE II-4.  Percentage of Samples Exceeding 20 ug/1 of Lead at Different
*- 	
Age of House
0-2 years


2-5 years


6+ years


F§
£6.4
7.0 - 7.4
>8.0
<6.4
7.0 - 7.4
>8.0
<6.4
7.0 - 7.4
<8.0
Percent of
First-flush
93%
83%
72%
84%
28%
18%
51%
14%
13%
samples >20 ug/1
Fully-flushed (2 min)
51%
5%
0%
19%
7%
4%
4%
0%
3%
Source:  U.S. EPA  (1987), preliminary results  fron "Lead Solder Aging Study"

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                               11-45





 seems to continue to produce relatively high levels of contami-



 nation even in relatively non-corrosive waters (e.g., Neilsen,



 1976).  The preliminary results from the EPA solder study on pH



 adjustment, however, indicate that even these levels can be



 reduced significantly through treatment.



      For this  analysis, we assumed that the  best  treatment cur-



 rently available will be adequate  to reduce  lead  levels to



 20  ug/1, except perhaps in certain specific  circumstances such



 as  first-flush waters that have been standing for  16 hours or



 more,  or with  lead  solder  that  is  under  two  years  old.






 Assumption;  EPA will change  its monitoring  requirements to better



 detect corrosion by-products  in drinking water.  The common inter-



 pretation of EPA's  current monitoring  requirements  calls for



 fully-flushed  samples,  typical  of  distribution water.*   Such prac-



 tice will not  capture the  presence of  lead in drinking  water,  or



 indeed,  the presence  of  any corrosion  by-products,  and  results  in



 underestimations  of contamination  and  exposure.  This analysis



 assumes  that EPA  will change  its regulations  to capture  that



 exposure  and that the criteria  for compliance with  the  new MCL



 will consider  the risk of contamination  by corrosion by-products.



 A revision of  EPA"s monitoring requirements was called  for by  the



 court  in  the decision on a  lawsuit brought by the Environmental



 Defense Fund against  the Agency, as EPA  accumulated data on the
*  This issue is discussed at the beginning of Section II.B.

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                              11-46





factors likely to affect lead levels in drinking water.  EDF v.



Costle, 578 F.  2d 337, 349-350 (D.C. Cir. 1978).  It was also



clearly the intent of the National Primary Drinking Water Regula-



tions  (40 CFR §141.2(c)) and the Preamble to the Regulations (FR,



volume 40, number 248, p. 59575 - December 24, 1975) that corrosion



by-products be addressed.  These revisions have been expected



by the regulated community (e.g., AWWA Committee Report, 1984)



and by professionals  in the  field  (e.g., Hoyt et al.,  1979;



Patterson  and O'Brien,  1979) for several years.





Assumption;  Adults  consume  2  liters of water  (or  water-based



fluids) per day  and  children consume 1 liter per day.   For



consistency with past analyses, this document  used the estimates



that  are  commonly  held  in  the  published literature and that have



served as exposure indexes  in  past EPA actions.





Assumption;   Lead  levels  are tap  specific.   Because the level  of



lead  contamination depends  largely upon  the  length of  contact



time  between  the water and  the plumbing  as  well as the parameters



of the water,  the  particular materials of the  private  and  public



plumbing  systems,  and the age of  the plumbing, lead levels vary



 from  tap to tap within a system and even  within a house.





Assumption;  The relationship between lead in drinking water and



 human blood-lead levels.  The published  literature presents



 several possible equations  relating lead levels in human blood to



 intake of lead from drinking water.  This analysis uses the

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                               11-47


 formulae  presented  in  the  Quantification of Toxicological Effects

 Section of  EPA's  Water  Criteria Document (1985)  for  lead, which

 are  taken from  the  Air  Quality Criteria Document (U.S.  EPA,  1986):


      (for children)  PbB* = 0.16**  x intake  of  lead  from water

      (for adults)    PbB* = 0.06**  x intake  of  lead  from water.


 The  coefficient for  children  is taken  from  Ryu (1983) ,  and the

 source of the coefficient  for  adults is Pocock (1983).   Both

 assumed a linear  relationship  between  lead  in  drinking  water

 and  blood lead levels.

      Two  other general  approaches  exist.  The  constant  used  for

 children  (PbB = 0.16 x  Pb  in water)  is  derived from  a study  of

 infant blood lead levels (Ryu,  1983) ,  in  which the "constant" was

 really a  non-steady  state  value.   This  may  be  an  inappropriate

 value to  use or may be, at best, a  lower  bound  estimate.t  A

 better "constant" may be the steady state value  from the control

 group in  the Ryu study, which  was  0.45.   If so,  the  projections

 of children's health effects in  this analysis  may be underestimated

 by as much as a factor of  3.

     Other studies of the relationship  between blood lead  levels

 and water lead concentrations  (cf.  the  discussion and bibliographic

 citations in the Air Quality Criteria Document, 1986, p.  Il-106ff.)
*   PbB = blood lead level

**  These constants have a unit of ug/dl per ug/day.

t   The authors of the Air Quality Criteria Document and the
    Water Criteria Document are aware of this problem.

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                              11-48

for both children and, more commonly, adults, have found cube
root functions, typically with intercepts of 4-7 ug/dl (blood
lead, with water lead = 0).  While the linear forms cited above
and used in this analysis provide results similar to the non-linear
forms over a very wide range of values (up to, say, 300 ug/1 of
water), the form of the model greatly influences the estimated
contributions to blood lead levels from relatively low water-lead
concentrations.  Over the typical range of lead levels in U.S.
drinking water  (0-100 ug/1) , the differences in estimated blood
lead levels can be quite large.  Indeed,  in  the range of this
analysis  (generally, water  lead levels of 0-50 ug/1), various
cube-root  functions yield values that are 4-10 times greater than
the estimates using the linear form  presented above.  Alternative
assumptions  (e.g., those reasonably  derived  from  the results of
Richards  and Moore, 1982 or 1984) could  indicate  that exposure —
and consequently benefits —  in this analysis may be underestimated,
possibly  by  several factors.
      Studies  investigating  the relationship  between  lead  in
drinking  water  and lead  in  the blood have found  a better  fit
between blood  lead levels  and lead  levels in standing or  first-
flush samples  than other measures  of lead contamination  of  water,
for  instance,  fully  flushed samples  (Worth  et al.,  1981;  Pocock
et al., 1983;  Bailey  and  Russell,  1981).   This seems counter-
 intuitive at first because the  intake of standing water  would  be
expected  to be much  less in total  volume consumed than  for  other
water (e.g., partly  or fully flushed water), so the expected

-------
                               11-49


contribution of the relatively high lead levels  typical of  standing

samples should be  small.  But  several studies  (Rabinowitz et al.,

1976 and 1980, in  particular)  have shown that  the absorption of

lead varies depending on the state of the gastrointestinal  system.

Specifically, lead ingested on an empty stomach  (e.g., at breakfast

or between meals)  has a much higher absorption rate than does

lead ingested on a full stomach.  This could explain the closer

correlation between blood lead levels and lead levels in standing

or first-flush water.

     Where studies have related blood lead levels to several

different measures of drinking water lead, the correlation

coefficient is larger for the  running samples than for the  first-

flush samples, generally by a  factor of 1.5-2  (e.g., Worth  et al.,

1981; Central Directorate on Environmental Pollution Study, 1982).

Whatever measure of water lead is used (first-flush, fully-flushed,

etc.), the corresponding coefficient of relationship to blood

lead must be used.  That means, if lead levels in partly flushed

water are measured, the coefficient should also be for partly

flushed samples.*  However, no studies calculated the relationship

between blood lead levels and lead levels in partly flushed

water.  This analysis, therefore, uses the best.available analyses,

the Ryu and Pocock studies discussed above, which evaluated

first-flush water.  The use of the coefficients for first-flush
*  No study has yet calculated a value relating blood lead levels
   to an integrative measure of water consumption patterns, i.e., a
   measure reflecting actual drinking habits.  A new epidemiological
   study to derive such a coefficient would be necessary in order to
   use data on actual consumption patterns.

-------
                              11-50

water with occurrence data relating to contamination levels in
partly flushed water introduces a downward bias to the estimates.
     In general, the studies assessing the form of the blood-lead/
drinking-water-lead relationship, especially the British studies,
assume no contribution to the body burden of lead from any other
environmental sources besides drinking water.  (The major exception
is Worth et al., 1981.)  For infants, this may be a less significant
omission than for toddlers or adults.  Curiously, the authors of
these studies do not question why there is an intercept of 4-7
ug/dl, even if water lead is zero.  However, gasoline lead is an
important determinant of human blood-lead levels  (cf. Air Quality
Criteria Document for Lead, 1986, p. ll-42ff; Chapter 3 of The
Costs and Benefits of Reducing Lead in Gasoline,  1985; and sources
cited there).   Indeed, the reduction of gasoline  lead levels in
the United States in the late 1970s appears  to have resulted in a  .
reduction in children's blood-lead levels of almost half during
that period  (Annest et al., 1983).  Lead paint, under certain
conditions, can also result in high localized contamination
levels.
     Analyses of the contributions from various media to human
blood-lead levels,  focusing upon  exposures typical  in this
country, indicate that drinking water lead may account for about
14-55 percent of the total burden of lead.
     It  is most likely that drinking water contributes 15-40
percent  of the  lead body burden  (cf, discussions  throughout the
Air Quality  Criteria Document, summarized pp. 13-26ff).

-------
                               11-51


      This  analysis  employs  the Ryu and  Pocock coefficients (dis-

cussed  above)  relating  lead  levels in drinking water  to blood

lead  levels;  these  are  combined "with the  drinking  water lead

levels  presented  in this chapter  to calculate the  potential

effect  upon blood lead  levels.  These changes are  projected onto

extrapolations of the data  from the Second  National Health and

Nutrition  Examination Survey (NHANES II)* on  the distribution of

blood lead levels in the country  (cf, Air Quality  Criteria Document,

chapter 11) to predict  the health  benefits  that would  result from

a potential reduction in the MCL  from 50 ug/1  to 20 ug/1.


Assumption;  New solder containing  lead (under 24  months)  contri-

butes an average of 25 ug/1 of lead to drinking water.  Many

field and  laboratory studies have  found that  lead  solder alone ~

when used with copper household plumbing — could  easily produce

lead levels in drinking water well  above the current MCL,  even in

relatively non-corrosive waters.  To be conservative, we assumed
*  The NHANES II was a 10,000 person representative sample of the
   U.S. non-institutionalized population, aged 6 months to 74
   years.  The survey was conducted by the (U.S.) National Center
   for Health Statistics (NCHS)  over a 4-year period (1976-1980).
   The data base is available from NCHS and analyses of the
   lead-related data from it have been published before (e.g.,
   Annest et al., 1982 and 1983; Mahaffey et al., 1982a and 1982b-
   Pirkle and Annest, 1984).

   These extrapolations incorporate the reductions in exposure
   resulting from the current phasedown in lead in gsoline (the
   limit is currently 0.1 grams  of lead per gallon of gasoline).
   The projections developed in  support of that rule-making and
   presented in The Costs and Benefits of Reducing Lead in Gasoline
   (U.S. EPA, 1985b)  form the basis of the projections developed
   for this potential rule.

-------
                              11-52

that new solder would on average produce lead levels at half the

MCL, i.e., 25 ug/1, in partly flushed tap water.

Assumption;  People drink partly flushed tap water.*  Lead levels

are highest in first-flush samples, that is, in water that has

been sitting for several hours or more  (for instance, overnight

or all day).  But those conditions occur only infrequently  (at

most, once or twice per day for each faucet), and the sparce

data available on actual drinking water use patterns indicate

that the bulk of consumed water is partly  flushed  (e.g., Bailey

and Russell, 1981).  The likelihood of  flushing the water before

using it probably  follows age and  sex patterns, and those most at

risk of lead's adverse health effects — children  — may be least

likely to  flush the water.
     Therefore, EPA has  concluded  that  people  are  more  likely  to

consume partly  flushed water than  fully flushed water.
     On the other  hand,  two particular  demographic trends  over

the past  few decades  are likely to result  in an increase  in the

amount of lead from drinking water to which people are exposed.

First,  the number  and proportion of women working outside the

home has  increased from 40 percent in 1970 to 51.9 percent in

 1983 (Statistical  Abstracts,  1985? Tables 27,  658, 659, and

 elsewhere).  This  means that more homes will have two  'first-

 flushes'  per day — one in the morning and the other when the
 *  Or its equivalent:  Some first-flush and some fully flushed
    water.

-------
                               11-53



 parent(s)  return from work.*  Obviously, this doubles the possi-


 bility of exposure to high first-flush lead levels.  The second

 demographic trend that is significant is the decrease in the


 average number of occupants per  housing unit.  in 1950, there


 were, on average, 3.37 people per housing unit, which has decreased

 to 2.73 in 1983 (Statistical Abstracts, 1985; Table 54).  The


 number of  occupants of a dwelling is inversely proportional to


 lead levels in the drinking water,  probably because fewer occupants

 mean the water will,  on average,  remain in  the pipes longer.


      In addition,  as  noted above  in the discussion of the rela-

 tionship between blood lead levels  and levels of  lead in drinking

 water,  blood lead  levels  correspond best with first-flush or

 standing levels.



 Uncertainty;   Factors  affecting lead  levels  in multi-family

 housing, especially high-rise buildings.  The available  data  on


 lead  contamination  at  the  tap comes primarily from  single-family


 homes.   It  is  unclear  how  lead concentrations in multi-family

 housing  will vary.  in  the  absence  of  good data, there are


 three hypothesized  possibilities:   lead  levels  will be higher  in


 high-rises than  in  single-family homes with similar water, lead

 levels will be lower, or contamination levels  and patterns will


 be the same.  There are plausible arguments to  support each thesis.


     Lead levels may be higher in high-rise buildings because  it

 is more difficult, and perhaps impossible, to fully flush the
*  Exposure to lead in the work place or at school is not included
   in this analysis.

-------
                              11-54





water in a building that is more than a few stories.  Because the



water is never really flushed, average residence time in pipes is



longer and therefore contamination levels will be greater.



     On the other hand, lead levels may be lower because one of



the factors contributing to high lead levels in tap water is the



relatively close ratio of water volume to surface area of pipe



resulting from the narrow pipes typical of home plumbing.  While



the pipes going to each faucet may be comparable, high-rise



buildings have service pipes that are, on average, much wider



than the largest pipes in homes.  Because of the reduced  ratio of



water to pipe surface  area, the potential for high lead contamina-



tion may be lower.  Another factor, number of occupants,  also cor-



relates inversely with lead levels.  Because multi-family housing



has more occupants in  total, average residence  time  for water in



pipes may be  shorter than  in single  family homes.



     The third possibility  is  that both  arguments above are



correct, and  that  they cancel  out.   Contamination levels  in  large



apartment buildings would  be comparable  to levels in single-family




homes.





II.C.2.  Calculations  of  Exposure  to Lead  in  Drinking Water



      Several  adjustments  to the available  data  on lead levels  in



tap  water  and in  new housing  are  necessary  to predict the number



of people  served  by  community water  supplies  who are likely to  be



exposed  to  drinking  water exceeding  an MCL of 20 ug/1.  These



 include the assumptions  discussed  above and  other data on the

-------
                               11-55


 composition of the housing stock in the United States and the use

 of various  plumbing materials.

      These  estimates are  for  one sample year  only,  1988.   Because

 the ban  on  the use of materials  containing  lead in  public water

 supplies will  become enforceable after  June 1988, exposure to lead

 in new housing can be expected to begin to  decrease, thereafter.


 II.C.2.a.   Estimate of Exposure  to Lead in  Drinking Water to
            Inhabitants of  New Housing     ~              ~~—

      The published literature shows that inhabitants of new housing

 are  at risk  of exposure to high  levels  of lead in drinking water.

 The  rates are  highest for  the first two years,  but  they decline

 and  are  generally  not elevated beyond five  years.

      There were 1.7 million new  housing  starts  and  permits in  the

 United States  during  1983  and 1.8  million in  1984.*   Construction

 data  show that housing  typically takes  six months to a year from

 permit to potential occupancy, so  there  are currently about 3.5

million  new housing units  (i.e.,  <  24 months).  The  Statistical

Abstract of the United  States (1985) indicates  that  in 1983,  the

average household  contained 2.73  individuals  (Table  58).   Multi-

plied together, a  total of 9.6 million people currently live  in

new housing.

     However, not  all of these people are served by  community

water supplies.  Of the current  (1985)  U.S.  residential population
*  Survey of Current Business, U.S. Department of Commerce -
   Bureau of Economic Analysis, 1985; Table on New Housing
   Construction.

-------
                              11-56


(a little over 240 million), 219.2 million are served by community

water systems and this analysis only addresses that population.

In addition, the use of plastic plumbing materials has increased

recently and voluntary switching to lead-free solder has occurred

in many areas; these homes are obviously at decreased risk of

exposure to lead from the leaching of new lead/tin solder.  Data

from the plumbing supply industry  show that about 8 percent* of

new plumbing is plastic,** so 92 percent of the population has

metal pipes.  We assumed that virtually all those with metal pipes

also have some solder or other fittings containing lead, although

this may overestimate exposure somewhat.  We  assumed that the

inhabitants of new housing are distributed proportionately between

community and non-community  water  supplies.   Therefore,  the

number of people served by community water supplies at risk of

high lead levels from new solder  in new housing  is:


                    219 million
         9.6 mil x  240 million  x  .92  =8.1 million people.


     This estimate,  based upon  the current population  and current

building practices,  is  for  one  sample  year,  1988.   The ban  on  the

future  use  of materials  containing lead  in public  water  supplies
 *    This is the arithmetic average of claims by the Plastic Pipe
     institute presented in Mruk (1984)  and of the Copper Develop-
     ment Association presented in Anderson (1984)„

 **  Plastic pipes are used more commonly for waste water than for
     intake water.  But the use of plastic pipes for both is
     increasing rapidly.

-------
                               11-57


and  in  residences connected  to them,  established  by  the  Safe

Drinking Water Act  as amended  in  1986, will  be  enforceable  after

June 1988.  Exposure to  lead  in new housing  can be expected to

decrease thereafter.


II.C.2.b. Estimate  of Exposure to Lead in Drinking Water  to
          Inhabitants of Older Housing

     The data on partly  flushed kitchen  tap  samples  indicate that

16 percent of the drinking water  in housing  older than two  years

in this country may exceed an  MCL of  20  ug/1.   To avoid double

counting, the inhabitants of new housing served by community

drinking water systems must be subtracted from  the total  number

of people served by community  water supplies.

     Of the current (1985) U.S. residential  population of a little

over 240 million, 219.2 million are served by community water

systems.  Again, we assumed that the  people  who live in new

housing (9.6 million)  are distributed proportionately between

community and non-community water supplies.  Therefore,


                       219 million
         9.6 million x 240 million  =8.8 million people.


To calculate the risk to inhabitants of older housing, subtract

the number in new housing (8.8 million)  from the total served by

community water systems  (219.2 million);  that indicates that

210.4 million people live in older homes.  Based upon the Culligan

data, 16 percent of them (33.7 million)  are  at-risk of high lead

levels in partly flushed water at their  kitchen taps.

-------
                              11-58


II.C.2.C.  Total Estimated Exposure to Lead in Drinking Water

     Combining the available data on lead levels in older housing

(33.7 million people exposed to lead levels >_ 20 ug/1) with the

new housing exposure estimates (8.1 million people at risk)

indicates that 41.8 million people using public water supplies

currently may be exposed to some water that exceeds the proposed

MCL of 20 ug/1; we round this to 42 million.

     This estimate is for one sample year, 1988.  Many uncertain-

ties surround this estimate, indicating that it may be high or

low.  Overall, exposure to lead in drinking water is  expected to

decrease somewhat after 1988 because of the Congressional ban on

the future use of pipes, solder and flux containing lead  in public

water systems and in residences connected to them.

     On  the other hand, this may be a low estimate

          0  because it does not include the potential exposure
             of occupants in housing built within the past 2-5
             years;*

          0  because we have not included those who,  while living
             in older housing, have recently had major plumbing
             repairs and so are also at risk of the potentially
             high lead levels associated with newly-installed
             solder;

          0  because the Culligan data represent water that  is
             harder than average, whereas high  lead levels are
             often  found with soft waters;
    The  incremental  risk  to  inhabitants  of  2-5  year  old  housing  is
    not  included  in  this  analysis  because  it was  not possible to
    eliminate  those  people  from  the  base and thus avoid  double-
    counting.

-------
                               11-59
           0  because the data used are for partially flushed
              samples, while some people (especially children)
              may consume water that is closer to first-flush
              or standing samples;* and

           0  because some of the statistical and analytical
              techniques used lend a downward bias to the results
              (e.g.,  the method of sample preservation and the
              use of  a first-flush correlation coefficient with
              data on lead levels in partly-flushed water).


      In  addition, we have not included any data from the estimated

 60 million people served wholly or in  part by private and non-

 community  water supplies.**
**
Blood lead levels are more closely related to lead levels
in first flush or standing water.

Some people are served by both public and private supplies.
For instance, a person's home may be served by a public water
system while the drinking water supply at school or work may
be private.                                                J

-------

-------
                             CHAPTER III
          BENEFITS OF REDUCING CHILDREN'S EXPOSURE TO LEAD

      The scientific literature presents evidence of a variety of
 physiological effects associated with exposure to lead,  ranging
 from relatively subtle changes in various biochemical measure-
 ments at very low levels of exposure, to severe retardation
 and  even death at very high levels of exposure.  Although such
 effects  are  found in individuals of all ages,  particular concern
 has  focused  on children.
      Because the  body is a  complex structure of interdependent
 systems  and  processes,  effects upon one component will have cascad-
 ing  implications  throughout the body.   This interdependence is
 well  illustrated  by multi-organ impacts resulting from the  inhibi-
 tion  of  heme synthesis  by lead,  with consequent reduction in the
 body  heme pool.   These  effects are depicted graphically  in  Figure
 III-l, taken from EPA's most  recent Air Quality Criteria Document
 for Lead (1986; p.  13-31).  A summary of children's  health  effects
 from  exposure  to  lead,  taken  from  the  Air Quality Criteria  Document
 and included in the  Water Criteria Document for Lead (1985),
 p. VIII-65,  is also  included  here  as  Figure III-2.
      This chapter  summarizes  the available evidence  of the  effects
 of lead  on children, and estimates  some  of the  health benefits of
 reducing exposure  by reducing  lead  concentrations  in drinking water.
 Section A deals with the pathophysiological effects of lead,
while Section B addresses the  evidence on neuropsychological
effects  (primarily reduced cognitive ability),  and Section C
discusses the fetal effects of lead exposure.   Section D presents

-------
                            III-2

   Figure  III-l   Multi-Organ Impacts of Lead's
                      Effects on  the  Heme Pool
REOUC
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           Multi-organ impact of reductions of heme body pool by lead. Impairment of home
synthesis by lead                 results in disruption of a wide variety of important physio-
logical processes in many organs and tissues. Particularly well documented are erythropoietic,
neural, renal-endocrine, and hepatic effects indicated above by solid arrows (—^-). Plausible
further consequences of heme synthesis interference by lead which remain to be more conclu-
sively established are indicated by dashed arrows (	*-).

-------
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-------
                              III-4





the methods used to monetize the benefits of reducing children's



exposure to lead.  Section E discusses some inherent limitations



of eost-of-illness studies, upon which most of these monetized



health benefits are based, and lists many additional health



effects that are not included at all in our analysis.  A summary



of the monetized and non-monetized children's health benefits



for one sample year (1988) is presented in Section F.



     Fuller discussions of the adverse health effects associated



with lead exposure can be found in other EPA documents: the Air



Quality Criteria for Lead (1986), including the Addendum which is



part of Volume 1; the Quantification of Toxicological Effects



section of the Drinking Water Criteria Document on Lead (1985);



and The Costs and Benefits of Reducing Lead in Gasoline (1985).



     This document rests heavily upon the analysis and



methodologies in The Costs and Benefits of Reducing Lead in



Gasoline.  Two sections  (III.A.4 on Stature Effects and III.C.



on Fetal Effects)' have been expanded from the earlier analysis;



the other sections have been condensed.  This reflects the



inclusion of new materials and is not an indication of relative



importance.  In addition, this document  includes  an alternative



method  for valuing one aspect of cognitive damage:  potential



decrement  in IQ, valued  as a function of the potential decrease



in  future  earnings.  This chapter  also  contains  a discussion of



the limitations  of cost-of-illness  studies, both  in general and



of  the  specific  studies  which serve as  the basis  of  this analysis,



that did not appear  in the earlier  cost  benefit  analysis.

-------
                               III-5

     The  estimates  of  health  benefits  associated  with this
proposed  rule  rely  upon  data  on  the  distribution  of  lead  levels
in  children  and  adults collected as  part  of  the Second National
Health and Nutrition Evaluation  Survey (NHANES II).   The  NHANES  II
was a 10,000 person representative sample of the  U.S.  non-institu-
tional! zed population, aged 6  months to 74 years.  The survey was
conducted by the  (U.S.)  National Center for  Health Statistics
(NCHS) over a  four-year  period (1976-1980).   The  data  base  is
available from NCHS and  analyses of  the lead-related  data from it
have been published before (e.g., Annest  et  al.,  1982  and 1983;
Mahaffey  et al.,  1982a and 1982b; Pirkle  and Annest,  1984).  This
survey provides careful  blood, biochemical,  nutritional and many
other biological, social, and  demographic measures representative
of  the U.S. population.
     The  fact  that  other sources  of lead, especially gasoline,
would slowly decline even without new  EPA drinking water  standards
created a slight  complication  in  projecting  blood lead levels for
sample year 1988.   Because gasoline lead  levels fall over time as
unleaded gasoline replaces leaded, the difference in blood lead
levels resulting  from this rule will change  over  time.  The
estimates in this report account  for both reductions in some
other sources  of  lead and changes in the  demographic profile of
the U.S.  population.  This model  served EPA  also  in its analytical
efforts supporting  the most recent phasedown  in the amount of
lead permitted in leaded gasoline; it  is discussed more fully in
The Costs and Benefits of Reducing Lead in Gasoline (US-EPA,
1985b).

-------
                               III-6

III.A.  Pathophysiological Effects
     Elevated blood-lead levels have long been associated with
neurotoxicological effects and many other pathological phenomena:
an article on lead's neurotoxicity was published as early as 1839,
on kidney damage in 1862, and on impaired reproductive function
in 1860.  From an historical perspective, lead exposure levels
considered acceptable for either occupationally-exposed persons or
the general population have been revised downward steadily as
more sophisticated biomedical techniques have shown formerly-
unrecognized biological effects, and as concern has increased
regarding the medical and social significance of such effects.
In the most recent downward revision of maximum safe levels (late
1984 - early 1985), the Centers for Disease Control (CDC) lowered
its definition of lead toxicity to 25 ug/dl blood lead and 35
ug/dl of erythrocyte protoporphyrin (EP).  The present literature
shows biological effects as low as 10 ug/dl (for heme biosynthesis)
or even 6 ug/dl (for fetal effects and for IQ effects in some
populations); indeed, some effects (e.g., elevated ALA levels,
hearing decrements, or stature effects) have exhibited no threshold
so far.
     There is no convincing evidence that lead has any beneficial
biological effect in humans (Expert Committee on Trace Metal
Essentiality, 1983).
     The finding of biological effects at the lowest observed
blood-lead levels (4-6 ug/dl) potentially has important implica-
tions for public health, because such levels are common in the

-------
                                III-7


U.S. population.  As Table III-l shows, between 1976  and  1980

over three-quarters of children under the age of 18 had blood

lead levels in excess of 10 ug/dl, and 15 percent exceeded 20

ug/dl.  The rates among blacks and among preschool children were

even higher.

     Lead's diverse biological effects on humans and  animals are

seen at the subcellular level of organellar structures and

processes, and at the overall level of general functioning that

encompasses all of the bodily systems operating in a  coordinated,

interdependent way.  The biological basis of lead toxicity is its

ability, as a metallic cation, to bind to bio-molecular substances

crucial to normal physiological functions, thereby interfering

with these functions.  Specific biochemical mechanisms include

lead's competition with essential metals for binding  sites,

inhibition of enzyme activity, and inhibition or alteration of

essential ion transport.  The effects of lead on certain subcellu-

lar organelles, which result in biochemical derangements common

to and affecting many tissues and organ systems (e.g., the disrup-

tion of heme synthesis processes),  are the origin of many of the

diverse types of lead-based functional disruptions of organ

systems.

     Lead is associated with a continuum of pathophysiological

effects across a broad range of exposures.  In addition to the

high level effects mentioned above, there is evidence that low

blood-lead levels result in:

       1.  Inhibition of pyrimidine-5'-nucleotidase (Py-5-N)
          and delta-aminolevulinic  acid dehydrase (ALA-D)
          activity,  which appears to begin at 10 ug/dl of

-------
                            III-8

TABLE III-l.  Blood Lead Levels of Children in the United States
              1976-80 (percent in each cell; rows sum to 100 percent)

All Races
all ages
6 months-5 years
6-17 years
White
all ages
6 months-5 years
6-17 years
Black
all ages
6 months-5 years
6-17 years
<10 ug/dl
22.1
12.2
27.6
23.3
14.5
30.4
4.0
2.7
8.0
10-19
ug/dl
62.9
63.3
64.8
62.8
67.5
63.4
59.6
48.8
69.9
20-29
ug/dl
13.0
20.5
7.1
12.2
16.1
5.8
31.0
35.1
21.1
30-39
ug/dl
1.6
3.5
0.5
1.5
1.8
0.4
4.1
11.1
1.0
40-69
ug/dl
0.3
0.4
0.0
0.3
0.2
0.0
1.3
2.4
0.0

-------
                        III-9
   blood lead or below  (Angle et al., 1982).
   Hernberg and Nikkanen  (1970) found 50 percent of
   ALA-D inhibited at about 16 ug/dl.

   Inhibition of erythrocyte ALA-D appears to occur at
   virtually all blood  lead levels measured so far, and
   any threshold remains  to be determined (cf, summary
   of literature in Air Quality Criteria Document, 1986;
   pp. 12-13 to 12-51).

2. Elevated levels of EP  zinc protoporphyrin (ZPP) in
   red blood cells at about 15 ug/dl.  This probably
   indicates a general  interference in heme synthesis
   throughout the body, including interference in the
   functioning of mitochondria (Piomelli et al., 1977).
   Changes in heme metabolism have been reported peri-
   natally at blood lead  levels of 8-10 ug/dl (Lauwerys
   et al., 1978).  Some studies that accounted for iron
   status show that children with low iron stores are
   more sensitive to lead in terms of heme biosynthesis
   interference (e.g., Mahaffey and Annest, 1986).

3. Changes in the electrophysiological functioning of
   the nervous system.  This includes changes in slow-
   wave electroencephalogram (EEC) patterns and increased
   latencies in brainstem auditory evoked potentials
   (Otto et al., 1981, 1982, 1984) which begin to occur
   at about 15 ug/dl.  The changes in slow-wave EEC
   patterns appear to persist over a two-year period.
   Also, the relative amplitude of synchronized EEC
   between left and right lobe shows effects starting at
   about 15 ug/dl (-Benignus et al., 1981).  Finally,
   there is a significant negative correlation between
   blood lead and nerve conduction velocity in children
   whose blood lead levels range from 15 ug/dl to about
   90 ug/dl (Landrigan et al., 1976).

4. Inhibition of globin synthesis, which begins to
   appear at approximately 20 ug/dl (White and Harvey,
   1972; Dresner et al., 1982).

5. Increased levels of aminolevulinic acid (ALA) in
   blood and soft tissue, which appear to occur at
   about 15 ug/dl and may occur at lower levels
   (Meredith et al., 1978).  Several studies indicated
   that increases of ALA in the brain interfered with
   the gamma-aminobutyric acid (GABA) neurotransmitter
   system in several ways (Criteria Document, 1986;
   p. 12-145 ff).

6. Inhibition of vitamin D pathways, which has been
   detected at the lowest observed blood-lead levels
   (Rosen et al., 1980a, 1980b; Mahaffey et al., 1982).
   Further, as blood lead levels increase, the inhibition
   becomes increasingly severe.

-------
                              111-10


       7.  An inverse relation between maternal and fetal
           blood-lead levels and gestational agef birth
           weight, and early post-natal development (both
           physical and mental) down to 10 ug/dl and possibly
           below (Bellinger et al., 1984; McMichael et al.,
           1986).  Investigations of post-natal growth and
           development also present evidence of a negative
           association with blood-lead levels at the lowest
           observed blood-lead level (Schwartz et al., 1986).

       8.  Finally, recent studies of IQ effects in poor
           black children (Schroeder, 1985; Schroeder and
           Hawk, 1986) show IQ effects over the range of
           6 to 47 ug/dl, without an evident threshold
           (cf also Air Quality Criteria Document, 1986;
           p. 12-92 ff, 12-157, and elsewhere).  Another
           recent article (Schwartz and Otto, 1987) shows
           hearing effects throughout the range of measured
           blood-lead levels.

These data cite the lowest observed effect levels to date, and

do not necessarily represent affirmative findings of thresholds

below which exposures can be considered safe.

     The specific effects listed above as occurring at blood lead

levels below 25 ug/dl indicate (a) a generalized lead impact on

erythrocytic pyrimidine metabolism,  (b) a generalized lead-induced

inhibition of heme synthesis,  (c) lead-induced interference with

vitamin D metabolism, and (d)  lead-induced perturbations  in

central and peripheral nervous system functioning.

     As lead exposure increases, the effects become more  pro-

nounced and broaden to additional biochemical and physiological

mechanisms in various tissues, causing more  severe disruptions

of the normal functioning of many organ systems.  At very high

lead exposures,  the neurotoxicity and other  pathophysiological

changes can result in death or,  in some cases of non-fatal lead

poisoning, long-lasting  sequelae such as mental  retardation  and

severe kidney disease.

-------
                                III-ll


      This  chapter  discusses  the known  pathophysiological  effects

 of  lead  that occur in  children,  particularly  the  neurotoxic  and

 fetal effects,  and the expected change in  the number  of children

 at  potential risk  of those effects  under EPA's proposed drinking

 water regulation.


 III.A.I.   Effects  of Lead on Pyrimidine Metabolism

      The best-known effect of  lead  on  erythrocytic pyrimidine

 metabolism is the  pronounced inhibition of Py-5-N activity,  an

 enzyme that controls the degradation and removal  of nucleic  acid

 from  the maturing  red  blood cell  (reticulocyte).  As  noted earlier,

 the disruption  of  this  function  by  lead has been  noted at exposure

 levels beginning at 10  ug/dl.  At blood lead  levels of 30-40

 ug/dl, this disturbance is sufficient  to materially contribute

 to red blood cell  destruction  and,  possibly,  decreased hemoglobin

 production contributing to anemia (World Health Organization,

 1977; National Academy  of Sciences, 1972? Lin-Fu, 1973; Betts et

 al.,  1973).  The mechanism of  this  inhibition may have a wide-

 spread impact on all organs and tissues.


 III.A.2.   Effects on Heme Synthesis and Related
          Hematological Processes

     These effects, are described more fully  in the Air Quality

Criteria for Lead  (EPA, 1986),  are only summarized here.

-------
                              111-12





III.A.2.a. Mitochondrial Effects



     The mitochondrion is an organelle within the cell and outside



the nucleus that produces energy for the cell through cellular



respiration and is rich in fats, proteins and enzymes.  It is the



critical target organelle for lead toxicity in a variety of cell



and tissue types, followed probably by cellular and intracellular



membranes.  The scientific literature shows evidence of both



structural injury to the mitochondrion (e.g., Goyer and Rhyne,



1973; Fowler, 1978; Fowler et al., 1980; Bull, 1980; Pounds et



al., 1982a and 1982b) and impairment of basic cellular energetics



and other mitochondrial functions (e.g., Bull et al., 1975; Bull,



1977, 1980; Holtzman et al., 1981; Silbergeld et al., 1980).



These and other studies also provide evidence of uptake of lead



by mitochondria in vivo and in Vitro.





III.A.2.b.  Heme Synthesis Effects



     The best-documented effects of lead are upon heme biosynthesis.



Heme, in addition to being a constituent of hemoglobin, is an



obligatory constituent for diverse hemoproteins in all tissues,



both neural and non-neural.  Hemoproteins have important roles  in



generalized functions, such as  cellular energetics, as well as  in



more specific functions such as oxygen transport and detoxification



of toxic foreign substances (e.g., the mixed-function oxidase



system  in the liver).  Statistically significant effects are



detectable at 10-15 ug/dl.



     The  interference of lead with heme synthesis in  liver mito-



chondria  appears to result in the reduced capacity of the  liver



to break down tryptophan, which,  in turn, appears to  increase

-------
                               111-13

levels of tryptophan and serotonin  in the brain  (Litman  and
Correia, 1983).  This may account for some of the neurotoxic
effects of lead.
     The elevation of aminolevulinic acid (ALA)  levels is another
indication of lead's interference in heme synthesis and  mitochon-
drial functioning.  Because increased ALA is associated  with
significant inhibition of certain kinds of neurotransmission,  such
elevations can have serious neurotoxic implications.  Thus, in
addition to its direct molecular neurotoxicity,  lead may adversely
affect the brain at low exposure levels by altering heme synthesis
(e.g., Silbergeld et al., 1982).  There appears  to be no threshold
concentration for ALA at the neuronal synapse below which presyn-
aptic inhibition of GABA release ceases.
     Since ALA passes the blood brain barrier and is taken up by
brain tissue, it is likely that elevated ALA levels in the
blood correspond to elevated ALA levels in the brain (Moore and
Meredith, 1976).  Furthermore, lead in the brain is likely to
enhance brain ALA concentrations because neurons are rich-in mito-
chondria, the subcellular site of ALA production.  As mentioned
earlier, blood ALA elevations are detectable at  18 ug/dl of blood
lead (Meredith et al., 1978).

III.A.3.  Lead's Interference with Vitamin D Metabolism  and
          Associated Physiological Processes
     Another potentially serious consequence of  lead exposure
is the impairment of the biosynthesis of the active vitamin D
metabolite, 1,25-(OH)2 vitamin D, detectable at blood lead
levels of 10-15 ug/dl.  Further, an inverse dose-response rela-
tionship has been reported between blood lead and 1,25-(OH)2

-------
                              111-14

vitamin D throughout the range of measured blood lead values up
to 120 ug/dl (Criteria Document, p. 12-37 ff.; Rosen et al.,
1980af 1980b; Mahaffey et al., 1982b).  Interference with vitamin
D production disrupts calcium and phosphorous homeostasis, par-
tially resulting in the reduced absorption of these elements from
the gastro-intestinal tract.  This may alter the availability of
these elements for physiological processes crucial to the normal
functioning of many tissues, cell membranes, and organ systems.
     The reduced uptake and utilization of calcium has two
compounding consequences.  First, it interferes with calcium-
dependent processes that are essential to the functioning of
nerve cells, endocrine cells, muscle cells (including those in
the heart and other components of the cardiovascular system),
bone cells, and most other types of cells.  The second concern
is possible increased lead absorption resulting from decreased
calcium availability.  The latter can be expected to further
exacerbate the inhibition of vitamin D metabolism and reduced
calcium availability  (Sorrell et al., 1977; Mahaffey et al., 1986),
resulting in even greater lead absorption and greater vulnerability
to increasingly more  severe lead-induced health effects (Rosen et
al.,  1980b; Barton et al., 1978).  These effects are especially
dangerous for young  (preschool age) children who are developing
rapidly.  These children, even  in  the absence of lead, require a
relatively high intake of calcium  to support  the formation  of the
skeletal system, as  well as several other calcium-dependent
physiological processes  important  in young children.

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                               111-15





      Even moderate levels of lead exposure in children are



 associated with vitamin D disturbances that parallel certain meta-



 bolic disorders and other disease states,  as well as severe kidney



 dysfunction (Criteria  Document,  1986;  p.  12-37).   At blood lead



 levels of 33-55 ug/dl,  1,25-(OH)2 vitamin  D is reduced to levels



 comparable to  those observed in  children who have severe  renal



 insufficiency  with the  loss  of about two-thirds of their  normal



 kidney function (Rosen  et al., 1980a;  Rosen and Chesney,  1983;



 Chesney et al.,  1983).   Analogous vitamin  D hormone depressions



 are  found in vitamin D-dependent rickets  (type I),  oxalosis,



 hormone-deficient  hypoparathyroidism,  and  aluminum intoxication



 in children undergoing  total parenteral nutrition.



      Lead-induced  interference with  1,25-(OH)2  vitamin D  biosyn-



 thesis  affects  a wide range  of physiological  processes.   The



 vitamin D-endocrine  system is responsible  in  large  part for  the



 maintenance of  extra- and  intra-cellular calcium  homeostasis



 (Rasmussen  and Waisman,  1983; Wong,  1983;  Shlossman et al.,  1982;



 Rosen  and  Chesney, 1983).  Thus,  modulation  in  cellular calcium



 metabolism  induced by lead at relatively low  concentrations may



 potentially disturb multiple  functions of  different  tissues  that



 depend  upon calcium as a second messenger  (Criteria  Document, p.



 12-40).  It also appears that 1,25-(OH)2 vitamin  D  participates



 directly in bone turnover by orchestrating the population of



 cells within the bone (Criteria Document,  p.  12-41).  An immuno-



 regulatory role for the vitamin D hormone  is  evident through the



widespread existence of 1,25-(OH)2 vitamin D3 receptor sites in

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                               111-16

immunoregulatory cells, such as monocytes and activated lymphocytes
(Provvedini et al., 1983; Bhalla et al.f 1983).
     The negative correlation between blood lead and serum
1,25-(QH)2 vitamin Df the hormonally active form of vitamin D,
appears to be another example of lead's disruption of mitochondrial
activity at low concentrations.  While serum levels of 1,25-(OH)2
vitamin D decreased continuously as blood lead levels increased
from the lowest measured level (12 ug/dl), this was not true for
its precursor, 25-(OH) vitamin D.  In fact, in lead-intoxicated
children after chelation therapy, 1,25-(OH)2 vitamin D levels
were restored, but the precursor levels remained unchanged  (Rosen
et al., 1980a, 1980b; Mahaffey et al.,  1982).  This indicates
that lead inhibits renal 1-hydroxylase, the kidney enzyme that
converts the precursor to the active form of vitamin D.  These
observations in children are supported  by lead effects on vitamin
D metabolism jln vivo  and in vitro  (Smith et al., 1981; Edelstein
et al., 1984).  Renal  1-hydroxylase  is  a mitochondrial enzyme
system, which  is mediated by the hemoprotein,  cytochrome P-450.
This suggests  that the damage  to the mitochondrial systems  detected
at 15  ug/dl and below has uncompensated consequences.
     If cytochrome P-450 is being  inhibited at the low levels  of
blood  lead that the  reduced renal  1-hydroxylase  activity suggests,
it is  possible that  other physiological functions  related to
cytochrome P-450  are also disrupted.   For example, reduced  P-450
content has been  correlated with  impaired activity of  the liver
detoxifying enzymes,  aniline hydroxylase  and  aminopyrine demethy-
lase,  which help  to  detoxify various medications and  xenobiotics

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                               111-17

 and modulate the metabolism of steroid hormones (Goldberg et al.,
 1978;  Saenger et al., 1984).
      While cytochrome P-450 inhibition has been found in animals,
 and in humans at higher lead levels, this has not yet been
 examined in children at blood lead levels < 25 ug/dl.  But the
 disruption of vitamin D biosynthetic pathways at these levels is
 suggestive of an effect.
     The reduction in heme  caused by lead exposure probably
 underlies the effects seen  in vitamin D metabolism.   This would
 explain  the similarity in the effect of lead on both  erythrocyte
 protoporphyrin accumulation and  decreases in levels of serum
 1,25-(OH)2D.   It would also indicate a  cascade of  biological
 effects  among  many organ and physiological  systems of the body
 (depicted graphically in Figure  III-l).   Together, the inter-
 relationships  of calcium and lead metabolism,  lead's  effects
 on  1,25-(OH)2D,  and  the apparent  disruption  of the cytochrome
 P-450 enzyme system  provide  a  single molecular and mechanistic
 basis for Aub  et al.'s observation in 1926 that  "lead follows
 the calcium stream."

 III.A.4.  Stature Effects
     Small stature has been  identified with  lead poisoning for
many years  (e.g., Nye, 1929), and is a plausible outcome, given
 the known biotoxic interaction of lead with calcium messengers,
heme-dependent enzymes, and neuroendocrine function.   Several
new studies provide evidence of a much stronger assooiation

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                               111-18

between exposure to lead and subsequent growth and development
than was previously thought.  These studies of stature effects
were not included in The Costs and Benefits of Reducing Lead in
Gasoline.  The Addendum to the Criteria Document (1986), appended
to Volume 1, contains a discussion of the deleterious effect of
lead upon various aspects of development and growth, even at
the relatively low exposure levels encountered by the general
population, i.e., 15 ug/dl and below  (p. A-31 to A-56).

III.A.4.a.  Effects of Lead on Fetal Growth
     Many studies have investigated the effect of intrauterine
lead exposure on gestational age, fetal growth and fetal physical
development.*  The Air Quality Criteria Document (1986? pp. 12-
192 to  12-220) and the Addendum  to the Criteria Document (1986;
pp. A-31 to A-56) contain a full review of these studies.
     Several studies examined the relationship between maternal
or fetal blood-lead levels  and gestational age.  Moore et al.
 (1982), for  instance, conducted  a cross-sectional study of  236
mother-infant pairs in Glascow,  Scotland.  Blood lead levels
showed  a significant negative relation  to gestational age,  for
both maternal and cord lead measures.   The blood lead levels were
within  the normal range  and higher,  with geometric mean blood-lead
 *  Many of these studies also show a relationship between blood
    lead levels (both maternal and fetal)  and negative pregnancy
    outcomes,  including early membrane rupture,  miscarriages_and^
    spontaneous abortions, potential minor congenital anomalies in
    live births, etc.  These and other adverse effects upon the
    fetus are discussed in Section III.C.  of this report.

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                               111-19

 levels of 14 ug/dl for the mothers and 12 ug/dl for the infants.
 As an indication of the findings, the mean blood-lead levels for
 the 11 cases of premature birth (gestational age under 38 weeks)
 were among the highest and averaged about 21 ug/dl for mothers
 and 17 ug/dl for infants.   in this study, first-flush household
 water lead levels were positively associated with both maternal
 and fetal blood-lead levels.
      In another recent study  of gestational age (McMichael et al.,
 1986), following 774 pregnancies to completion (live birth,
 spontaneous  abortion,  or still birth),  women with blood  lead
 levels >  14  ug/dl were over 4 times more  likely to deliver pre-term
 than  women with blood  lead levels  of <_  8  ug/dl.  Excluding cases
 of  still  births,  the relative risk increased to almost 9.
      Other studies  have  looked at  the relationship between prenatal
 exposure  to  lead  and birth weight  or size.   Nordstrom  et al.
 (1979b),  examining  records of female employees  of  a Swedish
 smelter,  found  decreased birth weights  related  to:   1) employment
 of  the mother at  the smelter  during pregnancy,  2)  distance the
 mother lived from the  smelter, and 3) proximity of  the mother's
 job to the actual smelting process.  In a related  study (Nordstrom
 et  al., 1978a), similar results were found for  infants born to
mothers merely  living  near the smelter.
     A more recent paper by Bryce-Smith (1986)  found both  birth
weight and head circumference related to placental lead levels
in a cohort of 100 normal  infants-.   Another study  (Bellinger et
al., 1984), studying mental development  in middle class children

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                              111-20


up to 2 years old, found a more subtle exposure-related trend in

the percentage of small-for-gestational-age infants.  Dietrich

et al. (1986), presenting interim results, also found that pre-

natal lead levels were associated with both reduced gestational

age and reduced birth weight, which  in turn were both signifi-

cantly associated with reduced neurobehavioral performance at

three months.

     Some other studies  (e.g., Clark, 1977; McMichael et  al.,

1986*) did not find  birth weight  statistically significantly

related to blood  lead  levels, however.   Nonetheless,  "the evidence

as  a whole from these  studies  indicates  that  gestational  age

appears to be reduced  as prenatal lead exposure  increases, even

at  blood  lead levels below  15  ug/dl" (Addendum  to the Criteria

Document,  1986; p.  A-45).

      Other recent studies  of lead's adverse effect upon physical

development  have  assessed  neurobehavioral aspects of child

development.  These studies are described and evaluated in  Section

 B on lead's  neurological effects.  Lead's adverse impact on

 gestational  age,  however,  has cascading effects upon subsequent

 mental development  in infants.


 III.A.4.b.  Effects of Lead on Post-Natal Growth

      The first article on lead's effect on stature  (Nye, 1929)

 observed the incidence of "runting", eye squint and drop foot  as

 physical characteristics of overtly lead-poisoned children.
 *  The Addendum  to  the Criteria Document  (1986; p. A-43f)  suggests
    that  the  findings  of McMichael  et  al.  are  "not  entirely clear
    with  regard to birth weight.  The  proportion of pregnancies
    resulting in  low-birthweight singleton infants  [in the  high
    blood-lead group]  .  .  .  was more than  twice that  for  the [low
    blood-lead group]."

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                               111-21

 Since then, however, surprisingly few studies have investigated
 this effect, until quite recently.
      In the 1970s, three studies (Mooty et al., 1975; Johnson and
 Tenuta, 1979; Routh et al., 1979) investigated possible stunting
 of physical growth as an end point of lead exposure.   In the
 first study, the children in the high-lead group (blood leads of
 50-80 ug/dl) were shorter and weighed less than those in the
 low-lead group (blood leads, 10-25 ug/dl).  But the high-lead
 group was also slightly younger (average age 33 months vs.  average
 age 34 months in the low-lead group)  and not racially matched,  so
 it is difficult to determine clearly  the relative contribution  of
 lead to the difference  in stature.  Johnson and Tenuta studied
 the growth and diets of 43  low-income children and  also found a
 relative decrease in height  with an increase in blood lead  level.
 But they did not report the  specific  racial composition and mean
 ages of  the subjects, nor did  they assess  the  relative contribution
 of  differences in calcium intake or the  incidence of  pica or
 other  factors.   Routh and co-workers  found the  incidence of
 microencephaly (defined as head  circumference  at or below the
 third percentile  for the  child's  age  on  standard growth charts)
 was  markedly greater among children with blood  lead levels  >_ 30
 ug/dl than  in  those with  blood lead levels  below 29 ug/dl.
Again, however;  it is not possible to distinguish the  relative
 contribution of lead from other  (racial, dietary, etc.) factors
 that may have  affected  these children's growth.  Despite their
 individual weaknesses,  the three studies together are suggestive
of an effect.

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                              111-22

     Much stronger evidence for the retardation of growth and
decreased stature associated with exposure to lead has emerged
more recently from animal toxicology studies and the evaluation
of large epidemiologic data sets.
     About 65 papers on animal experimental studies have been
published in the last 10 years that investigated the retardation
of growth following low-level exposure during intrauterine life,
early post-natal life or both.  These studies found decreased
body weight at blood lead levels of 18-48 ug/dl with no change
in food consumption (e.g., Grant et al.,  1980).  Deficits  in
the rate of neurobehavioral development and indications of specific
organic or functional alterations were observed at blood  lead
levels as low as 20 ug/dl  (e.g., Fowler et al., 1980).  As
summarized in the Addendum to the Criteria Document  (1986; p. A-
51),  "it seems very clear  [from  these animal  studies]  that low-
level chronic lead during  pre-  and  early  post-natal  development
does  indeed  result  in retarded  growth even  in the  absence of
overt signs  of  lead  poisoning."
      Finally, Schwartz  et  al.  (1986)  analyzed results  from the
Second National  Health  Assessment  and  Nutritional  Evaluation Survey
 (NHANES II)  to  investigate the  relationship between blood lead
 levels and physical development, controlling for other contri-
 buting factors,  including  age,  race,  sex, several measures of
 nutritional status,  family income,  degree of urbanization and
 many other variables enabling them to account for general health,
 and environmental and nutritional factors that might not be
 adequately controlled for by the nutrient and blood measurements.

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                               111-23

 To assure that blood lead was not found to be significantly
 associated with growth and development because of the correlation
 between blood lead and nutritional status, a stepwise regression
 procedure employing potential confounding variables  was used.
 To address the NHANES  II  survey design,  the computer program
 SURREGR was used.
     Schwartz's results show  that blood  lead levels  are a
 statistically significant predictor  of children's height (p  <
 0.0001),  weight (p < 0.001) and  chest  circumference  (p  < 0.026),
 after controlling  for  age (in months), race,  sex  and nutritional
 covariates.
     Figures  III-3  and III-4  illustrate  the  relationship of  stature
 (height  and weight) to blood  lead, after controlling for all of
 the other covariates.  The threshold regressions  (using  segmented
 regression models)  indicate that  there is  no  identified  threshold
 for the relationship down to the  lowest  observed blood lead of 4
ug/dl.   The relationship  is consistent through the normal range
 (5-35 ug/dl).

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                                     111-24
     FIGURE III-3   Relationship  of Blood Lead  Level to
                       Weight in Children Aged 0 to 7
ADJUSTED
WEIGHT (Kg>
      	5	              10          16       20     K     M
                             ADJUSTED BLOOD LEAD W
-------
                                       111-25
    FIGURE III-4   Relationship  of Blood Lead  Level  to
                      Height in Children Aged 0 to 7
                               ADJUSTED BLOOD LEAD 
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                               111-26


     At the average age (59 months), the mean blood-lead level of

the children appears to be associated with a reduction of about

1.5 percent in the height that would be expected if their blood

lead level was zero.  The relative impact on weight and chest

circumference is of the same magnitude.


III.A.4.c.  Summary of Stature Effects

     The inverse correlation of blood lead and growth in U.S.

children is often understood in the  context that blood lead is a

composite  factor for genetic, ethnic, nutritional, environmental,

and socio-cultural  factors that are  insufficiently delineated by

age,  race,  sex and  nutrition or by  family  income, urban residence,

and all other available nutritional  indices.  An environment that

favors  a higher blood  lead* may supercede  all of the  established

predictors such as  socioeconomic  status  and other demographic

characteristics.

      Growth is a complicated phenomenon,  accompanied  by an  orderly

sequence  of maturational  changes.  There are many mechanisms  that

may account for  lead's effect  on  physical growth and  development.

Prenatal  exposure  has  an  inverse  effect on gestational  age, which
 * Assessments of the risk of ambient lead exposure recognize the
   triple jeopardy of the urban poor: 1) the exposure to lead from
   multiple sources is highest in low income areas; 2) in high lead
   environments, the amount ingested increases with deficiencies in
   child care and household cleanliness; and 3) the intestinal
   absorption of lead increases with nutritional deficits.  The
   interaction of socio-cultural and nutritional deprivation with
   both environmental exposure and absorption of lead has long
   confounded the delineation of the threshold for behavioral and
   cognitive effects of low-level lead exposure.

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                                111-27

 in turn can adversely affect growth.   There are known negative
 interactions between lead and calcium messengers,  heme-dependent
 enzymes,  and neuroendocrine function.  While the effect is clearly
 plausible,  little  research has investigated potential mechanisms
 directly.   At least  one  very recent article (Huseman et al.,  1987)
 uses  a  rat  pituitary model to support the  biological plausibility
 of a  neuroendocrine  effect on growth.
      At 20  ug/dl,  vitamin D metabolism is  potentially sufficiently
 disrupted to hamper  the  uptake and  utilization  of  calcium,  and
 children are one-and-a-half times more likely to exhibit  abnormal
 red blood cell  indices than at 10 ug/dl.   For this analysis,  we
 have  assumed that  children with blood lead levels  over 20  ug/dl
 are at  risk  of  suffering  from smaller stature.   To assess  the
 benefit of  this potential  rule, we  used the  NHANES data on  the
 distribution of blood lead levels in  the country to  calculate the
 number of children who would  be brought below 20 ug/dl of blood
 lead  at an MCL of  20 ug/1:  82,000.
      We have ascribed no monetary value to this  health effect
 because it  is difficult to put  a monetary  value  on gestational
 age,  fetal development, and children's growth and stature.  The
 correlation with blood lead level is  independent of  the significant
 effects on growth of sex,  race, and nutritional  status, as well
 as all identifiable measures of socioeconomic status.  As yet,
 it has exhibited no threshold.  Common sense, however, suggests
 the value would be high.
     The method used to calculate the number of fetuses at risk
of exposure to potentially dangerous  levels of lead  is described
 in Section C, below.

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                               111-28





III.B.  Neurotoxic Effects of Lead Exposure



     Lead has been known to be a neurotoxicant since the early



1800s, and neurotoxicity is among the more severe consequences



of lead exposure.  At very high blood-lead levels, encephalopathy



and severe neurotoxic effects are well documented; the neurotoxic



effects at lower blood-lead levels, however, are less clearly



defined.  Recent research has investigated the occurrence of



overt signs and symptoms of neurotoxicity and the manifestation



of more subtle indications of altered neurological functions  in



individuals who do not show obvious signs of lead poisoning.



     This section presents new data on cognitive effects at low



levels of lead exposure.  These studies were not discussed in



The Costs and Benefits of Reducing Lead in Gasoline.





III.B.I.  Neurotoxicity at Elevated Blood-Lead Levels



     Very high blood-lead levels  (i.e., above 80 ug/dl  in



children) are associated with massive neurotoxic effects that



can include  severe,  irreversible  brain damage; ataxia  (i.e.,  the



inability to coordinate voluntary muscular movements);  persistent



vomiting; lethargy;  stupor;  convulsions;  coma; and  sometimes



death.   Once encephalopathy  occurs,  the risk  of  death  for  children



is significant  (Ennis and Harrison,  1950; Agerty,  1952;  Lewis et



al.,  1955),  regardless of  the  quality of  the  medical treatment



they  receive.

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                                111-29

       In  cases  of  severe  or  prolonged  nonfatal  episodes  of  lead
 encephalopathy, the neurological damage  is qualitatively
 similar  to that often seen  following  traumatic or  infectious
 cerebral injury, with permanent and irreversible damage being
 more  common in children  than adults (Mellins and Jenkins,  1955;
 Chisolm, 1956, 1968).  The most severe effects are cortical
 atrophy, hydrocephalus (an abnormal increase in cranial fluid),
 convulsive seizures, and severe mental retardation.  Permanent
 central nervous system damage almost always occurs in children
 who survive acute lead encephalopathy and are re-exposed to
 lead (Chisolm and Harrison,  1956).   Even if their blood lead
 levels are  kept fairly low,  25-50  percent show severe permanent
 sequelae including seizures, nervous disorders, blindness,  and
 hemiparesis  (paralysis of half  of  the  body)  (Chisolm and Barltrop,
 1979).
      Even children without obvious  signs  of acute  lead
 encephalopathy  have exhibited persisting  neurological damage.
 As  early  as 1943,  Byers and  Lord's  study  of 20  previously "lead-
 poisoned  children  indicated  that 19  later performed unsatis-
 factorily in school, "presumably due to sensorimotor  deficits,
 short  attention span, and behavioral disorders".  Effects such
 as mental retardation, seizures, cerebral palsy, optic atrophy,
 sensorimotor deficits, visual-perceptual problems,  and behavior
 disorders have been documented extensively in children following
 overt lead intoxication or even just known high exposures to
 lead (e.g.,  Chisolm and Harrison, 1956; Cohen and Ahrens, 1959;
Perlstein and Attala, 1966).

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                               111-30

      The extent of the later manifestations seems to relate to
the severity of the earlier observed symptoms.  In Perlstein and
Attala, 9 percent of the children studied, none of whom appeared
to have severe symptoms when diagnosed for overt lead poisoning,
were later observed to be minimally mentally retarded and 37
percent showed some lasting neurological sequelae.
     At somewhat lower blood-lead levels (i.e., 30-70 ug/dl),
substantial data confirm that a variety of neural dysfunctions
occur  in apparently asymptomatic children.  Several studies
indicate that blood lead levels of 50-70 ug/dl are associated
with IQ decrements of 5 points.  Adverse electrophysiological
effects, including markedly abnormal EEC patterns, slow-wave
voltages, etc.,  are also well documented at  levels of 30-70
ug/dl  and even below.
     De la Burde and Choate  (1972, 1975) showed persisting  neuro-
behavioral deficits  in  children  exposed  to moderate-to-high levels
of lead; most  of the children appear to  have  had  blood  lead levels
>_ 50 ug/dl.  Compared  to  low-lead  control  children — matched  for
age, sex,  race,  parents'  socioeconomic status,  housing  density,
mother's  IQ, number  of  children  in the family below  age 6,  presence
of father in the home,  and mother working  — the  higher lead
children  averaged  about five points  lower in IQ and  were seven
 times  more likely to have repeated grades in school  or to have
 been referred  to school psychologists.  Moreover, follow-up studies
 showed that these effects persisted for at least three years.
      The 5-point IQ decrement found in asymptomatic children with
 blood lead levels _> 50 ug/dl is consistent with other studies.

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                               111-31


 These include Rummo (1974) and Rummo et al. (1979), which found a

 16-point decrement in children > 80 ug/dl and a 5-point loss in

 asymptomatic children averaging about 68 ug/dl, and reanalysis

 by Ernhart of the data in Perino and Ernhart (1974) and Ernhart et

 al. (1981), as described in the Criteria Document (US-EPA, 1986;

 p. 12-81 to 12-85).*

      While chelation therapy may mitigate some of these persisting

 effects, significant permanent neurological and cognitive damage

 results  from very high lead levels,  with or without encephalopathy.

 In addition, these children also appear more likely to experience

 neurological and  behavioral impairments later  in childhood.


 IH.B.2.   Neurotoxicity at Lower Blood-Lead Levels

      The adverse  effects  of lead on  neurological functioning,  both

 on the microscopic (e.g.,  cellular and  enzymatic) level and  the

 macroscopic  (e.g.,  learning behavior) level, are well  documented.

 On the micro-level,  data  from  experimental  animal studies  suggest

 several  possible mechanisms for  the  induction of neural effects,

 including:   (1) increased  accumulation  of ALA in the brain as  a

 consequence  of lead-induced impaired heme synthesis, (2) altered

 ionic balances and movement of ions across axonal membranes and

 at nerve terminals during  the  initiation or conduction  of nerve

 impulses due to lead-induced effects on the metabolism  or synaptic

utilization of calcium, and (3) lead-induced effects on the

metabolism or synaptic utilization of various neurotransmitters.
*  Ernhart submitted the re-analysis, with better control for
   confounding variables and with errors corrected, to EPA's
   Expert Committee on Pediatric Neurobehavioral Evaluations (1983).

-------
                              111-32

     In addition, lead-induced heme synthesis impairment, resulting
in reduced cytochrome C levels in brain cells during crucial develop-
mental periods, has been clearly associated with the delayed develop-
ment of certain neuronal components and systems in the brains of
experimental animals (Holtzman and Shen Hsu, 1976).  (Cytochrome C
is a link in the mitochondrial electron transport chain that pro-
duces energy, in the form of adenosine triphosphate  (ATP), for the
entire cell.)  Given the high energy demands of neurons, selective
damage to the nervous system seems plausible.
     In addition to the effects of lead on the brain and central
nervous system, there is evidence that peripheral nerves are
affected as well.  Silbergeld and Adler (1978) have  noted lead-
induced blockage of neurotransmitter  (acetylcholine) release in
peripheral nerves  in rats,  a possible result of lead's disruption
of the transport of.calcium across cellular membranes.  This
disruption of cellular calcium transport may also  contribute to
the  effects  of  lead on peripheral nerve conduction  velocity.
Landrigan et al.  (1976) have noted  a  significant correlation
between blood  lead and decreasing nerve conduction velocity  in
children  in  a  smelter community.  This effect may  indicate  advan-
cing peripheral neuropathy.
     Paralleling  these cellular  or  biochemical  effects  are
electrophysiological  changes  indicating  the perturbation of peri-
pheral and  central nervous system functioning  observed  in children
with blood  lead levels of  15  ug/dl  and  even below.   These include
 slowed nerve conduction  velocities  (Landrigan et  al.,  1976),
 reaction-time  and reaction-behavior deficits (Winneke  et al.,  1984;

-------
                                111-33


 Yule,  1984), as well as persistent abnormal EEC patterns including

 altered brain stem and auditory evoked potentials down to 15 ug/dl

 (Benignus et al.,  1981; Otto et al.,  1981, 1982, 1984).  Neuro-

 logical effects of lead at such low levels are particularly

 important because  two- and five-year  follow-up studies (Ot,to et

 al.,  1982,  1984)  indicated some persistent effects.

     A recent article (Schwartz and Otto,  1987)  has  confirmed

 earlier findings of hearing effects related to low and moderate

 lead exposure.  This study also found lead levels significantly

 related to  major neurological milestones  in early childhood

 development,  including the age  at  which a  child  first  sat up,

 walked  or spoke.   No threshold  was evident for either  the hearing

 or developmental effects.

     Animal  studies have also noted aberrant learning  behavior

 at lower  blood-lead levels.  Crofton  et al.  (1980) found  that the

 development  of  exploratory behavior by  rat pups  exposed to  lead

111 utero  lagged behind  that  of  control  rats.   Average  blood-lead

 levels  on the 21st  postnatal day were 14.5  ug/dl*  for  the exposed

pups and  4.8 ug/dl*  for the  controls.

     Gross-Selbeck  and Gross-Selbeck  (1981)  found  alterations in

the operant behavior of adult rats after prenatal  exposure  to

lead via mothers whose blood lead  levels averaged  20.5  ug/dl.*  At

the time of testing  (3 to  4 months, postnatal),  the lead-exposed

animals' blood-lead levels averaged 4.55 ug/dl*  compared  to 3.68

ug/dl*  in the controls.  This suggests  that changes in  central

nervous system function may persist for months after the  cessation
*  Blood lead levels in animals are not comparable to human blood-
   lead concentrations.

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                               111-34

of exposure to relatively low blood-lead levels.  In addition,
animal studies show that behavior effects include both reduced
performance on complex learning problems and signs of hyperactivity
and excessive response to negative reinforcement (Winneke, 1977
and 1982a).
     Finally, these effects show signs of a dose-response relation-
ship.  In children with high level lead poisoning, neurological
damage is indisputable and mental retardation is a common outcome.
For children with somewhat lower blood-lead levels, de la Burde
and Choate  (1972, 1975) found lesser but still  significant cognitive
effects,  including lower mean IQs and reduced attention spans.
Several studies have found smaller effects at lower blood-lead
levels.   Some very recent studies have also shown previously-
undetected, significant cognitive effects  in poor black children
in the normal range of blood lead levels  (from  6 ug/dl) without
exhibiting  an evident threshold.
     While  some of these effects have only been observed  at
higher blood-lead  levels,  in animals, or  in vitro,  they show a
consistent  dose-dependent  interference with normal  neurological
functioning.  Furthermore,  several  of these effects have  been
documented  to occur at very  low blood-lead levels  «  10 ug/dl)
 in  children,  with  no  clear  threshold yet  evident.

 III.B.2.a.   Cognitive Effects  of Lower  Blood-Lead  Levels
      The earliest  study  of  cognitive effects  from relatively low
 levels of lead  exposure  was done by Needleman et al.  (1979),
 using shed deciduous  teeth from over 2,000 children to index lead
 exposure.  Among other findings, this study showed evidence of a

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                               I.II-35





continuous dose-response  function  relating  lead  levels  to  behavior



as rated by the  teacher in  terms of attention  disorders.   The



authors also divided  the  subjects  into  a  high- and  low-lead



group; significant effects  (p  < 0.05) were  reported for various



IQ indices, for  classroom behavior, and for several experimental



measures of perceptual-motor ability.   Numerous  papers  by  Needleman



and his co-workers have provided additional analyses and follow-up



studies related  to the original data.   These are listed in the



bibliography of  this  document  and  are summarized in the Criteria



Document (1986;  p. 12-85  ff).



     There were  many  questions relating to  the Needleman analysis.



An Expert Committee on Pediatric Neurobehavioral Evaluations,



convened by EPA, noted some methodological  problems  and asked for



a reanalysis and some additional analyses (Expert Committee,



1983).  Reanalyses were conducted  by Needleman (1984),  Needleman



et al. (1985) and EPA.  All of the reanalyses  confirmed the



published findings of significant  associations between  lead



levels and IQ decrements.   After controlling for confounding



variables, the Needleman data show evidence of a 4  IQ-point



decrement associated with blood levels  of 30-50  ug/dl.  This



finding is consistent with earlier studies  showing  IQ decrements



of 5 points or higher in children with  blood lead levels >^ 50



ug/dl discussed previously (de la Burde and Choate,  1972 and



1975; Rummo,  1974; Rummo et al., 1979;  etc.).



     Since Needleman's original study in 1979,  many other analyses



of cognitive effects related to low and moderate lead exposure have



been published.  While some of these studies,  like the earlier

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                              111-36


ones, suffer from some methodological flaws and the relatively

small sample sizes in many of them made it difficult to prove

a statistically significant effect,* the combined weight of the

studies point to "various types of neural dysfunction in apparently

asymptomatic children across a broad range of blood lead levels"

(Criteria Document, 1986;  p. 12-156), including small IQ decre-

ments in children with blood lead levels of 15-30 ug/dl.

     In addition, new studies have examined neurotoxic effects in

younger children and infants.  Section A (above) discussed results

from studies that found an inverse association between blood lead

levels and gestational age at blood lead levels found commonly in

the general population.  Because gestational age can affect

mental development in infants, whatever mechanism lies behind

that effect must be factored into the discussion of lead's neuro-

logical effects.
*  A statistical method for combining comparable studies to
   overcome the problem of small sample size  is described  in The
   Costs and Benefits of Reducing Lead in Gasoline  (EPA, 1985),
   p. IV-33 ff.

   For use in public policy making, rejecting the results  of
   studies simply because they  fail to attain significance at  the
   5 percent level may be inappropriate for two reasons.   First,
   policy makers need to be concerned about both type  I and type
   II errors.  Significance tests guard only  against the first
   type  (falsely rejecting the  null hypothesis of no effect);
   they help ensure that a regulation is not  imposed when  there
   is no adverse effect.  Type  II errors (failing to reject the
   null hypothesis when it is false) also can be costly, however,
   because they can result in the underregulation of a real
   hazard.  With small sample sizes and subtle effects, the
   probability of a type II error can be large.

   The second reason for caution in rejecting the results  of these
   studies, particularly in this case, is that while several fail
   to attain statistical significance individually, they do show a
   consistent pattern:  the children in the higher  lead groups
   generally have lower mean IQs.

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                               111-37

     Several studies  assessed  the  relationship  between  blood  lead
levels at birth and the subsequent mental development of  the
infants.  Bellinger et al.  (1984), observing  216 middle-  and
upper-middle class children aged 6 months to  2  years in a pros-
pective longitudinal  study of  early developmental effects of
lead, found scores on the Bayley Mental Development Index (MDI)
inversely related to  umbilical cord blood-lead  levels.  The
subjects were divided into three groups with  mean blood-lead
levels of 1.8 ug/dl (the low group), 6.5 ug/dl  (midgroup), and
14.6 ug/dl (high).  Gestational age and some  other variables were
identified as confounders of the association  between cord blood
lead and the MDI;* these confounding (positive) associations
reduce the degree of  association between cord blood lead  and the
MDI.  Adjusting for confounding, and controlling for all  known
relevant factors, the difference in scores between the high and
low blood-lead level  groups was about 6 points  on the MDI.
Follow-up studies (Bellinger et al., 1985; 1986a; 1986b)  indicated
that the association  between cord blood-lead  level and MDI score
continued for at least two years; no association was found with
post-natal blood-lead level.
     Vimpani et al.  (1985), in a longitudinal study of almost 600
children at age 24 months, also found a statistically significant
relationship between blood lead levels in infants and their per-
formance on the MDI.   Ernhart et al. (1985 and  1986) investigated
prenatal lead exposure and post-natal neurobehavioral function,
*  That is because gestational age is also related to cord blood
   lead levels.

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                              111-38

as well.  Of the 17 neurobehavioral measures examined in the
Ernhart studies, three showed significant relationships to blood
lead levels.
     Interim results of a longitudinal study presented by Dietrich
et al.  (1986), observing inner-city children in Cincinnati, showed
evidence of an inverse relation between blood lead levels at
three months with performance on three major mental development
indexes, including the MDI.  But these interim findings showed an
association only for white infants.  This and other analyses have
also shown indirect effects on mental development and performance
through lead's effect on gestational age and/or birth weight (cf.
Addendum to the Criteria Document, 1986; p. A-35f).
      In addition, several studies show an association between
blood lead levels and other neurobehavioral patterns.  Ernhart
(1985 and 1986) showed that prenatal lead exposure correlated
with certain neonatal behavior such as jitteriness and hyper-
sensitivity, as measured on the Neurological Soft Signs scale.  A
follow-up study (Wolf et al., 1985) showed evidence that lowered
Bayley  MDI scores for one year olds was a sequela of the cord
blood-lead relation shown on the Neurological Soft Signs scale
after birth.  And Winneke et al.  (1985a) showed a significant
relationship between perinatal blood-lead levels and one measure
of psycho-motor ability at ages 6-7.
     Finally, two new general population studies (Schroeder et  al.,
1985; and Schroeder and Hawk, 1986) investigated low socio-economic
status  children with blood lead levels  in line with  (or  just
slightly higher than) levels in the general population,  controlling

-------
                                111-39

 for  socio-economic  factors,  age,  race,  etc.   The first study
 examined  104  lower  SES  children with blood  lead  levels ranging
 from 6-59  ug/dl  (mean about  30  ug/dl).   This  study found  a signi-
 ficant  effect (p <  0.01)  of  lead  upon  IQ, which  was sufficient to
 disrupt the normal  mother-child IQ  correlation.   The second study,
 replicating the  previous  study  with 75  low  SES black children
 showed  a highly  significant  relationship (p < 0.0008)  between  IQ
 and  blood  lead levels over the  low  to moderate range of 6-47
 ug/dl.  These studies suggest that  lower socio-economic status
 places  children  at  greater risk of  the  deleterious effects of
 low-level  lead exposure on cognitive ability, while confirming
 that  other factors  (maternal IQ,  home environment,  etc.)  are also
 closely related  to  IQ.
     Winneke  et  al.  (1985a and  1985b) also examined the predictive
 value of different  markers of lead  exposure for  subsequent neuro-
 behavioral development.  Of an  original  study of  383  children  at
 birth,  114 subjects were followed-up at  ages 6-7.   Mean blood-lead
 levels  (maternal and infant) had  been 8-9 ug/dl  (range: 4-31
 ug/dl).  Regression analyses showed that maternal  blood-lead
 levels  (related  closely to umbilical cord levels)  accounted  for
 nearly as much of the variance  in neurobehavioral  test  scores  at
 age 6-7 as did contemporary blood-lead levels.
     The combined results of available studies of cognitive effects
 at low and moderate lead levels present evidence of potential  IQ
decrements and other cognitive  impacts due to lead exposure at
blood lead levels found commonly  in the U.S. population; i.e., at
15 ug/dl and below,  and possibly as low as 6 ug/dl for  some groups
of children.

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                               111-40

III.B.3.  The Magnitude of Lead's Impact on IQ
     The studies summarized above indicate that among the cognitive
effects resulting from exposure to lead is a potential lowering
of children's IQs and a reduction in their ability to perform
well in school.  The latest draft of the Criteria Document (1986)
characterizes the evidence' as suggesting that, on average, blood
lead levels of 50 to 70 ug/dl could correlate with average IQ
decrements of five points, blood lead levels of 30 to 50 ug/dl
could be associated with a four-point decrement in IQ, and that
lead levels of 15 to 30 ug/dl could be related to IQ reductions
of one-two points (p. 12-156, 12-282, and elsewhere).  In Section
III.D, we monetize the benefits of reducing these effects using
the costs of compensatory education and potential decreases in
future earnings resulting from decreased IQ.
     These levels of effects may be associated with relatively
consistent and/or relatively long exposure periods, possibly even
several years.  Permanent IQ effects may result only from fairly
long periods of exposure, and a child who has a certain blood lead
level for a relatively short amount of time (perhaps, a few months)
may not suffer the full effect.  Because of this uncertainty, for
the effect upon decreased future earnings, we assumed conservatively
that a child must be at a certain lead level for 3-4 years before
permanent and irreversible IQ loss results.
     This is an extremely conservative assumption.  The data on
prenatal exposure (obviously limited to at most nine months) show
significant effects  (both physical and neurological) persisting
for two years or more.  Fetal development is arguably particularly

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                               111-41





vulnerable to disruption.  Nonetheless, much data suggest that



post-natal exposure periods of a year or so produce detectable



effects.  In addition, even if a lead-induced lag in cognitive or



physical development were no longer detectable at a later age,



this does not necessarily mean that the earlier impairment was



without consequence.  Given the complex interactions that contri-



bute to the cognitive, emotional, and social development of



children, compensations in one area of a child's development may



exact a cost in another area.  Unfortunately, very little is



known about how to accurately measure these interdependencies.



We have chosen the conservative estimate of 3-4 years of exposure



because of unanswered questions of reversibility and permanence.



     The approach of ascribing benefits only to those children



who are brought below a critical threshold (15 ug/dl, 30 ug/dl or



50 ug/dl) by this proposed rule suffers from several faults,



which cut in opposite directions and may offset each other.



Categorization does not account for the fact that some children



who are prevented by the regulation from going over a given



threshold will do so by a narrow margin (e.g., their blood lead



level will be 29 ug/dl when it would have been 31 ug/dl in the



absence of the rule); such children are unlikely to receive the



full four-point gain in IQ but they will receive more than one



point.   This means that the benefits of this potential rule may



be overestimated.



     On the other hand, categorization attributes no benefit to



children whose blood lead levels are reduced from very high levels,

-------
                               111-42

but not brought below a given threshold or to those whose levels
would have been between two thresholds without the rule, but
whose levels decrease further by the reduction in lead in drinking
water.  Also, it is quite possible that children suffer long-
lasting, even permanent, effects with shorter exposure periods
than the 3-4 years we assumed.  These factors indicate that our
benefit estimate may be too low.

III.C.  Fetal Effects
     Lead's adverse effects upon human reproductive functions have
been known for over 100 years.*  In  1860,  for instance, Paul
published findings  (cited in the Criteria  Document, p. 12-192)
that lead-poisoned women were likely to abort or deliver stillborn
infants.  Because lead passes the placental  barrier and fetal lead
uptake continues throughout development, a growing concern  in
the public health community is  that  the most sensitive popula-
tion for  lead exposure  is fetuses and newborn infants.  This
concern is supported by both animal  and human studies.
     Several categories of  fetal effects were discussed previously,
Within Section A, above,  in the discussion of lead's  adverse
effect upon  children's  physical growth  and development, we
presented data on the  inverse relationships  between blood  lead
levels and gestational  age, birth weight  and birth height.
Section B, also  above,  describes  the neurotoxic  effects of  lead,
including the  inverse  relationship  between blood lead level and
 *  Indeed, 'lead plasters'  were used as abortifacients at the turn
    of the century.

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                                111-43





 infant mental  development  as measured  by  several  different



 neurological indices.




      In  addition,  several  studies  have implicated lead  in compli-



 cations  of  pregnancy,  including early  and still births,  and,



 possibly, low-level congenital  anomalies.   (Lead's adverse  effects



 upon  reproductive  function are  discussed  in  Section IV.B. of  the



 next  chapter.)  As discussed previously,  lead has a negative



 effect upon gestational age.  As early examples of these findings,



 Fahim et al. (1976) found  that  women who  had normal full-term



 pregnancies had average blood-lead levels  of 14.3 ug/dl, whereas



 women with  early membrane  rupture  had  average blood-lead levels



 of 25.6 ug/dl, and women with premature delivery  had average



 blood-lead  levels of 29.1  ug/dl.  Wibberly et al.   (1977) found



 that  higher lead levels in placental tissues were associated  with



 various negative pregnancy outcomes, including prematurity, birth



 malformation,  and neonatal death.  Bryce-Smith et al. (1977)



 found bone  lead concentrations  in still births of  0.4-24.2  parts



 per million (ppm) in the rib (average: 5.7)  versus  typical  infant



 bone  lead levels of 0.2-0.6 ppm.



     Needleman et al.  (1984) analyzed  data from over 4,000  live



 births at Boston Women's Hospital and  reported an  association



 between minor congenital anomalies and umbilical-cord blood-lead



 levels.   There was no association between  any particular malfor-



mation and  lead, but only  between all minor malformations and



 lead.  There also were no  significant  associations  between  lead



 and any major malformations, although given the rate of such



malformations in the general population, a sample this size has



 little power to detect such an effect.   Holding other covariates

-------
                               111-44

constant/ the relative risk of a child demonstrating a minor
malformation at birth increased by 50 percent as lead levels
increased from 0.7 ug/dl to 6.3 ug/dl (the mean cord-lead level).
This risk increased an additional 50 percent at 24 ug/dl.
(Umbilical-cord blood-lead levels are generally somewhat lower
than, but correspond to, maternal blood-lead levels; e.g., Lauwerys
et al., 1978.)
     Two other studies (McMichael et al., 1986; Ernhart et al.,
1985 and 1986) investigated the association between pre-natal
lead exposure and congenital morphological anomalies.  They did
not find a similar occurrence of congenital anomalies.  On the
other hand, the Needleman analysis relies upon a much-larger data
base than either the Ernhart or McMichael studies.  Nonetheless,
the available evidence on lead's effect  on congenital anomalies
allows  no definitive conclusion about low-level  lead exposures
and the occurrence of congenital anomalies.
     Finally, Erickson et al.  (1983) found lung-  and bone-lead
levels  in children who died from Sudden  Infant Death Syndrome
were significantly higher  (p < 0.05) than  in  children who died
of other causes, after controlling for age.   While  this  study
suggests a potential relationship between  lead exposure  and
Sudden  Infant Death Syndrome,  this  issue also remains to be more
fully  evaluated.
III.C.I.  Assessing the  Benefits of  Reduced  Fetal Exposure  to  Lead
     Lead  crosses  the  placental  barrier  and  fetal uptake of  lead
continues  throughout development.   Petal and  new-born blood-lead

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                               111-45


 levels  are  closely  related  to,  though  generally  slightly  lower

 than, maternal levels.*   In addition,  during physiological  condi-

 tions of bone dimineralization, which  are  known  to  occur  during

 pregnancy and lactation,  lead  as well  as calcium may be released

 from its storage  in bone.   A readily mobile compartment of  skeletal

 lead has been demonstrated  in  humans (Rabinowitz et al.,  1977) and

 in experimental studies both In vivo (Keller and Doherty, 1980a

 and 1980b)  and in vitro (Rosen, 1983;  Pounds and Rosen, 1986).

 For these reasons, to assess the benefits  of EPA's proposed reduc-

 tion in the MCL for lead, we are concerned with  two populations:

 pregnant women currently  at  risk of receiving high levels of lead

 in their drinking water and  especially those women  (aged  15-44)

who are likely to have blood lead levels that could present a

 risk to the unborn child.

     To determine what blood lead level should be used as a cut-

off for estimating risk to the fetus from  lead exposure,  two

recent policy actions related to EPA rules were considered.   In

the Spring of 1985, EPA's Clean Air Science Advisory Committee

recommended a goal of preventing children's blood-lead levels
*  "Exposure levels during the course of pregnancy may not be
    accurately indexed by blood lead levels at parturition.
    Various studies indicate that average maternal blood-lead
    levels during pregnancy may tend to decline, increase, or
    show no consistent trend.  These divergent results may simply
    reflect the likelihood that the maternal blood lead pool is
    subject to increase as bone stores of lead are mobilized
    during pregnancy and to decrease as lead is transferred to
    the placenta and fetus.  Apparently, then, under some condi-
    tions the fetus may be exposed to higher levels of lead than
    indicated by the mother's blood lead concentration."  (Text
    quoted from The Addendum to the Criteria Document, 1986; p.
    A-45.  See references cited there.)

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                              111-46

from exceeding 15-20 ug/dl.  This goal was supported by the
epidemiological and toxicological data at the time that showed
significant lead-induced health effects beginning to be detec-
table in that range.  More recently, the Addendum to the Criteria
Document (US-EPA, 1986; p. A-48) stated, "At present, . . . ,
perinatal blood lead levels at least as low as 10 to 15 ug/dl
clearly warrant concern for deleterious effects on early post-
natal as well as prenatal development."
     To be conservative, we used the intersection of these two
ranges — 15 ug/dl — as the blood lead level of concern for
fetal effects.  As the simplest relationship between maternal and
fetal blood-lead levels, we have assumed equivalence.  This
ignores some findings that the rate of  fetal absorption of lead
may  increase throughout development (e.g., Barltrop, 1969;
Rabinowitz and Needleman,  1982; Donald  et al., 1986).   (See the
Criteria Document, Sections 10.2.4  and  12.6, for a fuller dis-
cussion of this  issue.)
     The Air Quality Criteria Document  estimates that there are
approximately  54 million women  of childbearing age  (i.e., between
15  and 44 years  old), of whom about 7 percent are likely to be
pregnant at  any  given  time (1986; p.  13-47); this is about the
same percentage  as  the  annual birth rate  given by the Census
Bureau:  67.4  per  1,000 women aged  15-44.*   Census  Bureau  data
 (presented  in  Current  Population  Reports, Series  P-25,  or  summarized
 in  Table 27  in Statistical Abstracts,  1986)  show  that  24 percent
 *  1985 Statistical Abstracts of the United States (1986),
    Table 82.

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                                111-47


 of the total population is women aged 15-44.   Assuming that women

 of childbearing age and that pregnant women are distributed

 proportionately among those served by community water systems and

 by private  or non-community water supplies, and assuming that

 these  women are distributed proportionately between community

 water  systems with  high and low lead levels,  these figures yield

 the following estimates of fetuses at risk  of exposure to lead

 levels exceeding 20 ug/1 in drinking water.


   24%  x 42  million* x 67.4 per  thousand  = 680,000  fetuses at risk


     Calculating the  number of  women at  high  blood-lead  levels is

 more difficult.   Our  population models do not yet  include suffi-

 cient  data  on all adult women in the United States  because  our

 analyses so far  have  focused, separately, on  children  and adult

 men.   However, some data are available that enable  us  to  make  very

 crude  exposure estimates for this  population.

     The Hispanic Health and Nutrition Examination  Survey (called

 either  the  Hispanic HANES  or HHANES), conducted by  the National

 Center  for  Health Statistics (NCHS)  between 1982 and 1984 contains

 relatively  recent data  on  blood  lead  levels in the  U.S.,  including

 adults.  These data, published and available  from NCHS, indicate

 that in 1988 Mexican American women  aged 15-44 will have  an

estimated mean blood-lead  level of 7.1 ug/dl, with a geometric

standard deviation of 1.5; they also show that an estimated 0.36
*  Estimate of people in the United States served by community
   water supplies who currently receive water that exceeds 20 ug/1
   Methodology presented in Chapter II,

-------
                               111-48

percent of those women will have blood lead levels over 15 ug/dl
in 1988.*  While we do not know how data on Mexican Americans
compare to data on white Americans, these estimates certainly
significantly underestimate the lead levels of black Americans,
which are generally much higher than whites.**  Assuming that all
women in the U.S. have blood lead  levels and distributions comparable
to those in the Hispanic HANES:
                                 219
           54 million x 0.36% x  240 million = 177,000

women in 1988 served by community  water supplies  are  likely
to have blood lead  levels  over  15  ug/dl, of whom
                       177,000 x 7% =  12,400

are  likely to be  pregnant  in  any given year.   For these women,
any  contribution  of lead  from drinking water  is  a potential
health  risk  to  the  fetus  because they are  already at  the cut-off
point recommended by the  Clean  Air Science Advisory Committee,
and  the fetus may take the bulk of the lead absorbed  by the
mother.
      Determining  what fraction, if any,  of these most-at-risk
 fetuses (i.e.,  of mothers with blood lead levels > 15 ug/dl and
 receiving water > 20 ug/1) is included in the 680,000 at-risk
 *  These estimates rely upon the coefficients on the distribution
    of blood lead levels in the country from the NHANES II (dis-
    cussed previously) and Census Bureau data on the demographics
    of the population.  These extrapolations assume reduced
    exposure to lead from gasoline.
 ** For an indication of the racial differences in the distribution
    of blood lead levels, look at the data presented on Table III-l,
    on p. III-8 above.

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                                111-49

 fetuses  (i.e.,  of  mothers  receiving  water >  20  ug/1)  estimated
 above  is difficult.   To  avoid  double-counting we  have used the
 most conservative  and least  controversial assumptions   that all
 of  the most-at-risk  fetuses  are included  in  the 680,000 fetuses
 exposed  in utero to  drinking water exceeding the  proposed  MCL.
 Therefore, the  proposed  MCL  would protect 680,000 fetuses  in 1988.
    D.  Monetized Estimates of Children's Health Benefits
     The health benefits of reducing children's exposure to  lead
are diverse and difficult to estimate quantitatively or to value
in monetary terms.  The monetized benefits  include only two
admittedly incomplete measures:  savings in expenditures for
medical testing and treatment, and savings  associated with
decreased cognitive ability.  These measures of benefit exclude
many important factors, such as the reproductive and stature
effects discussed above.  These and other limitations are discussed
in Section III.E, below.
     In fact, many children with elevated blood-lead levels are
neither detected nor treated.  However, this estimation procedure
assumes that children who go undetected and untreated bear a
burden at least as great as the cost of testing and providing
the treatment (medical or educational)  of those who are detected.
So, all children with high blood-lead levels are assumed to incur
"costs"-, whether medical expenditure costs or personal costs in
the form of poor health, inadequate learning, decreased future
vocational options,  etc.

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                               111-50

III.D.I.  Reduced Medical Costs
     To estimate the benefits of reduced medical care expenses,
we used the optimal diagnosis, treatment, and follow-up protocols
recommended by Piomelli, Rosen, Chisolm, and Graef in the Journal
of Pediatrics (1984).  Piomelli et al. estimated the percentages
of children at different blood-lead levels who would require
various types of treatment.  Figure III-4 summarizes the treatment
options that we used, based on the recommendations of Piomelli
et al.
     An evaluation of typical medical services suggests that
administrative expenditures and follow-up tests would cost $110
(1985 dollars) for each child found to be over 25 ug/dl at screen-
ing.  Of those children over 25 ug/dl blood lead, based on Piomelli
et al.  (1982) and Mahaffey et al.  (1982), we estimated that 70
percent would be over 35 ug/dl EP.  Piomelli et al.  (1984)
recommend provocative ethylenediamine-tetraaeetie acid (EDTA)
testing for such children.  EDTA testing typically requires a day
in the  hospital and  a physician's  visit; based upon  hospital cost
data, we assessed a  cost of $540 per  test  (1985 dollars).  We
also  assumed that all children receiving EDTA testing would
receive a series of  follow-up tests  and physicians'  visits,
costing an estimated $330  (1985 dollars).
      The purpose of  EDTA testing is  to  see  if children have a
dangerously high body-lead burden  (a  lead  excretion  ratio  over
0.60, per Piomelli et al.).  Table III-2 presents Piomelli et  al.'s
estimates of the percentages of children at various  blood  lead
levels  who will require ehelation  therapy;  it ranges from  a

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                                    111-51
 FIGURE III-5.   Flow Diagram of Medical Protocols  for Children with Blood
 	Lead Levels above 25 ug/dl
               Blood Lead Levels
                  >25  ug/dl
                  elevated
                   FEP?
            no
                          yes
       sinple
       follcw-up
                              1
 high body
lead burden?*
                    no
     I
                                       yes
                 long
              follow-up
              chelation
               therapy
                                             I
                                          repeat
                                        chelation?
                                no
                                                        yes
                            long
                         follow-up
                             chelation
                              therapy
NOTES:

*Provocative EDTA or
 other test

tChelation therapy, because
 of its severe side-effects
 and inherent dangers,  cannot
 be repeated again after this
 point
                                                            I
                               repeat
                             chelation?
                   no
1
                                           yes
                long
              follow-up
         chelation
          therapy
                                                T
                                                                       long
                                                                      follow-upt

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                              111-52
TABLE III-2.  Percent of Children Requiring Chelation Therapy

          Blood Lead Levels 	Percent	
          25-30 ug/dl

          30-39 ug/dl
             age three and over
             age under three

          40-49 ug/dl
             age three and over
             age under three

          50-59 ug/dl
             age three and over
             age under three

          above 59 ug/dl
                                                    0*
  9.6*
 11.5*
 26.0
 37.9
 36.0
 49.0

100.0
 Source:  Piomelli  et  al.f  1984
    At blood lead concentrations of 25 to 35 ug/dl, 6-7 percent of
    children require ehelation therapy (Piomelli et al., 1984).
    The presentation above, while consistent with the data and
    other presentations, can easily result in an underestimation
    of risks.

    In addition, given the degree of non-linearity between blood
    lead levels and ehelatable lead, it is possible that some
    children between 15 and 24 ug/dl (a concentration below CDC's
    definition of 'elevated1 blood lead) may have positive EDTA
    test results.  Thus, the percentages above may represent
    conservative estimates.  (Based upon data and discussions with
    Dr. John Rosen, Department of Pediatrics, Montefiore Medical
    Center, Albert Einstein College of Medicine; one of the authors
    of the Piomelli article.)

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                               111-53

 low of zero for those tinder 30 ug/dl to a high of 100 percent
 for those over 59 ug/dl.
      Based on the data from the NHANES n, we estimated that,
 of those children over 25 ug/dl blood lead, about 20 percent are
 between 30 and 40 ug/dl and 10 percent are over 40 ug/dl.  Using
 those estimates and the percentages in Table III-2,  5 percent of
 the children above 25 ug/dl would require chelation therapy.
 In addition, we estimated that half of those children ehelated
 would require a second chelation due to a rebound in their blood
 lead level,  and that half of those children would require a
 third ehelation treatment.   Thus,  a total of 0.0875  ehelations
 would be  required  for every child  over 25 ug/dl  blood lead at
 screening.   To calculate the total cost per ehelation,  we estimated
 that it would  require five  days  in the  hospital,  several  physicians'
 visits, laboratory work,  and a neuropsychologieal  evaluation,
 for a  total  cost of about $2,700 per ehelation.
     Multiplying each of  these  costs  by  its  associated probability
 and then  summing them yields  the estimated  cost per  child  over '
 25  ug/dl:

     1.0($110) + 0.7($540) + 0.7($330) + 0.0875($2,700)= $955.25,

which we  round to  $950 in 1985 dollars.
     Because we have  not included welfare losses  (such as work
time lost by parents), the adverse health effects of ehelation
therapy itself (such as the removal of necessary minerals and
potential severe kidney damage), or such non-quantifiables as the

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                              111-54

pain from the treatment, this estimate of the benefits is conser-
vative.  As mentioned previously, these medical costs are a
measure of avoidable damage for all the incremental cases of lead
toxicity, whether detected or not.

III.D.2.  Costs Associated with Cognitive Damage
     The studies on the neurotoxicity of lead show a continuum of
effects, in a dose-response relationship, from low to high  levels
of exposure.  Manifestations of this neurotoxicity are varied and
include  IQ deficits and other cognitive effects, hearing decre-
ments, behavioral problems, learning disorders, and slowed  neuro-
logical  development.  Several of  lead's neurotoxic effects  can
combine, and a  few studies  (e.g., de la Burde and Choate, 1972,
1975)  show poorer performance in  school associated with  higher
blood-lead levels.  For  instance, these studies showed that
children with higher  blood-lead  levels were seven times  more
likely than  similar children with lower lead levels to repeat a
grade, to  be referred for psychological counseling, or to show
other  signs  of  significant behavioral  effect.   Supplementary
educational  programs  may compensate for  some of these effects,
though certainly not  all of them.
     Because of the  difficulties inherent in monetizing  neuro-
 logical effects, we  selected only one sub-category to investi-
gate further — cognitive damage resulting from exposure to lead.
We developed two methods for calculating the benefits of reduced
 cognitive damage:  compensatory education costs (as a proxy for
 the damage)  and decreased future earnings as a function of IQ
 points lost.

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                               111-55
 III.D.2.a.   Compensatory Education
      To estimate roughly the cost of compensatory education for
 children suffering low-level cognitive damage, we used data
 from a  study prepared for the Department of Education's Office of
 Special Education Programs.   Kakalik et al. (1981)  estimated that
 part-time special education  for children who remained in regular
 classrooms  cost $3,064 extra per child per year in  1978; adjust-
 ing  for changes in the GNP price deflator yields an estimate of
 $4,640  in 1985  dollars.   This figure is quite close to Provenzano's
 (1980)  estimate of the special education costs for  non-retarded,
 lead  exposed children.
      In developing the algorithm for calculating a  unit cost for
 compensatory education,  we made three relatively conservative
 assumptions.  First,  we  assumed that no children with blood  lead
 levels  below 25 ug/dl would  require  it.   This  is conservative
 because many studies  show detectable cognitive effects at  15 ug/dl.
 Second, we  assumed that  only 20  percent of  the children above 25
 ug/dl would  be  severely  enough affected to  require  and receive
 some compensatory  education.   Third,  based  upon several follow-up
 studies that  showed cognitive  damage  persists  for three years or
more  (even  after blood lead  levels have  been lowered),  we  assumed
 that each child who needed compensatory  education would  require
 it for three  years but that  the  damage  would then be  compensated
 for.   This  is conservative for two reasons.  As  a neurotoxin,
 lead affects many  capacities:  hearing, motor  coordination and
other sensory perceptions, as well as cognitive  abilities.  No
part-time in class special education  can possibly compensate for

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                              111-56

all these effects.  In addition, while no studies have yet been
published on this, data from several large lead poisoning preven-
tion programs (records on about 1,600 children treated at the
Montefiore Center in New York) show that once lead toxic children
require compensatory education, such educational services generally
will be required for many more than three years.  We have used
the three-year cut-off because the only published follow-up
studies show cognitive effects persisting for (at least) that
period of time.  Thus, the estimated average annual cost per
child over 25 ug/dl is
                 (0.20) x  (3) x  ($4,640) = $2,784,

which we round to $2,800  (1985 dollars), for compensatory education
to address lead's cognitive damage.

III.D.2.b.  Effect Upon Future Earnings
     Literature  concerning the economic returns  of  schooling has
included some  investigation of  the  impact of IQ  upon  earnings;  a
survey of this literature was prepared for  EPA by  ICF  (ICF,  1984)
and peer reviewed by  a panel  of  distinguished economists.   Typi-
cally, estimates of the returns  to  schooling are based upon an
 "earnings capacity" that  consists of  equations  for schooling,
 "ability"  (usually measured by  scores  on  standardized IQ tests),
 and  socioeconomic variables.   Both the main subject (economic
 returns  of  schooling)  and its off-shoot  (earnings  as  a function
 of IQ)  are  extremely  complicated and  controversial.
      Despite  the wide variety of data sets  and  methodologies used
 to examine  these issues,  the  estimates of the  direct effect of

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                                111-57

 ability on earnings appear to be fairly consistent.  With one
 exception, estimates of the direct effects of a one point change
 in IQ fall between 0.20 and 0.75 percent of future expected earn-
 ings.  There are fewer estimates of the indirect effects of IQ on
 future earnings (which include the impact of IQ on the schooling
 of the child,  which in turn affects expected earnings) and they
 range from 0.18 to 0.56 percent per IQ point.   Combined, a one
 IQ-point change is associated with a change of 0.65 to 1.15
 percent in earnings.   We used the arithmetic mean (one IQ point =
 0.90  percent of earnings)  to calculate the benefit of this rule.
      As summarized above (Section III.B.), the literature indi-
 cates that children with blood lead levels between 15 and 30  ug/dl
 could suffer IQ losses  of  1-2  points (for which we used  the arith-
 metic mean —  1.5  points —  as the  point  estimate),  between 30  and
 50 ug/dl children  could  lose  4 IQ points,  and  over 50 ug/dl they
 could lose 5 IQ  points.  Because  permanent IQ  damage probably
 occurs  after a year or more of lead  exposure,  we  assumed  conserva-
 tively  that  children would suffer these losses after 3-4  years  of
 exposure at these  levels.*  To calculate  the annual  benefits of
 this  proposed rule, therefore, the potential effect  upon  future
 earnings resulting from  these  exposure levels was divided by 3.5
years.  Multiplied together, reducing a child's blood-lead,level
below 15 ug/dl  could increase  expected future  lifetime earnings
by 0.4 percent
            (0.9% x 1.5 IQ points -? 3.5 years = 0.4%),
   Because recent data is showing that much shorter exposure periods
   produce effects that can last for at least 2-3 years, subsequent
   analyses will have to re-examine this assumption.

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                               III-5.8


reducing a child below 30 ug/dl could increase earnings by 1.0

percent
             (0.9% x 4 IQ points -s- 3.5 years = 1.0%),


and reducing a child below 50 ug/dl could increase earnings by

1.3 percent

             (0.9% x 5 IQ points f 3.5 years = 1.3%).


     The present value of expected lifetime earnings  is $687,150;*

deferred for 20 years at 5 percent real discount rate** reduces  it

to $258,950  (1985 dollars).  The effect of the cognitive damage

would decrease expected future earnings by $1,040  (1985 dollars)

for a child  brought below 15 ug/dl;  $2,600  (1985 dollars)  for

a child brought below 30 ug/dl; and  $3,350  (1985 dollars)  for  a

child brought below 50 ug/dl.

     To calculate  the annual benefits in  this  category, the

number of  children who would be brought  below  each of these

points  (15,  30  and 50 ug/dl) was multiplied  by the change  in

expected  future  lifetime  earnings.   Table III-3  presents  those

benefit calculations  for  the proposed MCL reduction to 20  ug/1

for  sample year 1988.
 *  Calculated from Bureau of the Census data:  Lifetime Earnings
    Estimates for Men and Women in the United States;  1979 (1983)
    — p.3 — and 1985 Statistical Abstracts of the United States
    (1986) — Table 216.  Converted to 1985 dollars.

 ** These costs are deferred because those suffering the effects are
    children and will not enter the work force for up to 20 years.
    Obviously, using the largest deferral period (20 years) reduces
    the value of the benefit and reduces the benefit estimate,
    whereas 8- or 10-year-old children may begin working within_8
    years and so would have a much shorter deferral period.  This
    biases the estimates downward slightly.

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                            111-59
TABLE II1-3.
Estimated Annual Benefits of Reduced IQ Damage
by Using Changes in Expected Future Lifetime
Blood Lead Level
Number of children
IQ points
potentially lost
Present value of
decreased earnings
(1985 dollars)
TOTAL
(1985 dollars)
15 ug/dl
230,000
1-2
per child
$1,040
per child
$239.2
million
30 ug/dl
11,000
4
per child
$2,600
per child
$28.6
million
50 ug/dl
100
5
per child
$3,350
per child
$ 0.3
million
TOTAL
241,100
NA
NA
$268.1
million

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                               111-60


III.D.3.  Summary of Monetized Benefits

     Table III-4 summarizes the estimates of the monetized annual

children's health benefits of the potential rule for one sample

year:  1988.  Adding the estimates of compensatory education

($2,800) and medical costs ($950) yields a combined annual benefit

estimate of $3,750 per case avoided of a child's blood-lead level

exceeding 25 ug/dl.  This  is Method 1 in Table  III-4.  Method 2

is medical expenses plus decreased future earnings as a consequence

of lead's adverse effect upon IQ.  The benefits of avoided cogni-

tive damage calculated as  a function of  IQ's relationship to

expected future  earnings are not  linear, however; they are a step

function.*  Therefore, average  costs per child  were not calculated.

Instead, we calculated the annualized benefit from avoided IQ

losses  of reducing  230,000 children  below  15 ug/dl; 11,000 children

below 30 ug/dl;  and 100  below  50  ug/dl,  and combined  that with

the  total medical  expenses avoided  for  bringing 29,000  children

below 25 ug/dl.  Note  that the  difference  between Method  1 and

Method  2  is that they  include  alternative  methods  for valuing

aspects of  the cognitive damage resulting  from  exposure to  lead.**

     The benefits  for  Method 1 (medical costs  plus  compensatory

education)  are not absolutely comparable to those  from Method  2,

 for three reasons.  First, Method 1 — based upon  per child

 estimates — is strictly a function of the number  of children
 *   Measurements were taken for the step function at 15 ug/dl,
     30 ug/dl, and 50 ug/dl.

 **  This biases the results downward because there is a strong
     rationale for considering these effects as additive.  Com-
     pensatory education is unlikely to fully compensate for the  _
     neurological damage caused by exposure to lead and so, effects
     upon future ability and performance could still result in
     decreased earnings.

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                                  111-61
TABLE III-4.  Monetized Annual Benefits of Reducing Children's Exposure to
              Lead Using Alternative Methods,  for Sample Year 1988
              (1985 dollars)


Number of
children
Costing
unit

Total
benefits

Medical
Expenses

29,000
$950
per child

$27.6
million
METHOD 1
Compensatory
Education Costs

29,000

Total
Method 1

29,000
$2,800 $3,750
per child per child

$81.2
million

$108.8
million

Medical
Expenses

29,000
$950
per child

$27.6
million
METHOD 2
Earnings
Lost

241,100
$268.1
million
total
$268.1
million

Total
Method 2

241 ,100
NA

$259.7
million

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                              111-62

passing one critical point:  25 ug/dl.  Method 2, on the other
hand, depends upon the distribution of children by blood lead
levels, and how the distribution changes* as a result of EPA's
proposed regulatory action.  Second, Method 1 ascribes no benefit
to any health effects below 25 ug/dl, while Method 2 includes
neurotoxic effects between 15 and 25 ug/dl.  Finally, Method 2
measures effects to a child over a working life, for each year of
exposure, while Method 1  includes only costs incurred for those
children who receive compensatory education for the duration of
that benefit.
     In addition, while they are discussed qualitatively, no
monetary value  is assigned to the fetal  effects,  the increased
risk of anemia, metabolic changes or  the negative impact upon
stature.  So the monetized benefit  estimates omit many  important
categories, and thus are  likely  to  be significant underestimates
of  the total benefits  of  reducing lead in drinking water.   The
next section contains  a discussion  of some of  these  factors.

III.E.  Valuing Health Effects;   Caveats and Limitations
     To begin  valuing  the health effects that  would  be  avoided  as
a result  of the new MCL  for  lead in drinking water,  we  estimated
1)  medical  treatment and  monitoring costs for  those  children whose
blood  lead  levels reach  or exceed the criteria recommended by
 the Centers for Disease  Control as  determining lead  toxicity
 *  That is, how many children pass each of several critical points,
    depending upon the category:  15 ug/dl, 25 ug/dl, 30 ug/dl or
    50 ug/dl.

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                                111-63

  (25 ug/dl of blood lead when combined with erythrocyte proto-
 porphyrin levels of 35 ug/dl), and 2) two alternative ways of
 valuing the cognitive damage resulting from lead exposure:
 the cost of part-time in-class compensatory instruction as a
 proxy for the cognitive damage that lead causes and decreased
 expected future earnings as a function of IQ loss.
      The cost-of-illness estimates themselves are low, primarily
 because, to reduce potential controversy, the calculations rely
 upon many conservative assumptions.  For instance, the monetization
 of compensatory education costs is based upon likely practice and
 not preferred treatment.   Although children suffering cognitive
 damage from lead exposure should  receive more intensive and
 extensive  educational  resources,  the  Department of Education
 estimated  that  they would probably receive  only part-time  in-
 class  remedial/compensatory help.   m  addition,  the  estimate  that
 only  20  percent  of children over  25 ug/dl would receive  any extra
 help  is  conservative.  The  real (social)  cost  of the illness  does
 not decrease  if  not all victims receive  the treatment  they need;
 assuming the  treatments are efficacious,  children who  are  left
 with diminished  cognitive abilities incur a cost at  least  equal
 to the cost of the treatment they  should  have  (but did not)
 receive.  The health benefit estimates, therefore, should  be
 understood as very low lower-bounds for these categories of
 effects.
     We have also not conducted cost-of-illness calculations for
most of the adverse health effects associated with human exposure

-------
                               111-64

 to lead.   Among the many effects not  valued monetarily in the
-health benefits analysis are:
      - kidney effects,  detectable in  children at about 10 ug/dl;
      - hematopoietic damage, detectable in children at below
        10 ug/dl;
      - neurological effects in children below the level of lead
        toxicity, with central nervous system effects detectable
        at below 10 ug/dl and no perceived threshold;
      - metabolic changes, detectable in children at about 12 ug/dl;
      - enzymatic inhibition, with no threshold  indicated in
        children, even below 10 ug/dl;
      - all effects on fetuses in vitro, although lead crosses the
        placental barrier and maternal blood-lead levels  correlate
        with  adverse pregnancy outcomes, including decreased
        gestational age, slowed mental and physical development
        in neonates, potential low-level congenital anomalies
        and other adverse outcomes, including  fetotoxicity at high
        levels;
       - stature effects  on  children,  which  are dose-dependent with
        no threshold  evident;  and
       - effects upon  other  organ systems,  for instance,  immune
        and gastrointestinal.
       Finally,  three  serious phenomena of  lead's adverse effect
  upon human health are  not  included.   First, hematopoietic,  meta-
  bolic, and enzymatic damages have cascading effects throughout  the
  body, which  are not adequately addressed.   Second,  many of the
  specific effects have  long-lasting sequelae that are not included.

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                               111-65

 And last, there is a significantly greater chance of serious
 effects later in life, including renal failure and neurological
 disorders, even in individuals whose highest detected blood-lead
 level was below that associated with the most severe effects and
 who did not at the time show evidence of lead toxicity; this risk
 is not included in the analysis.
      In addition to the categories of adverse health effects
 for which we have not yet been able to quantify benefits at all,
 the costs of the illnesses that  are calculated greatly underesti-
 mate the real (social)  benefits  of preventing those effects, even
 for the health categories evaluated.   The underestimates occur
 because of the exclusion  of some  categories  of direct costs
 associated with  those effects  and the total  exclusion of all
 indirect but related  costs (e.g.,  work  time  lost  by the parents
 of  lead-poisoned children).
     In general, "society's willingness-to-pay  to  avoid  a given
 adverse effect  is many  times greater  than the  cost  of  the  illness
 itself,  so cost-of-illness  analyses inherently underestimate the
 benefits of  avoiding  the  adverse effect.*  Willingness-to-pay
 studies  indicate that society  is usually willing  to pay  two -to
 ten times the cost of medical  treatment,  and that in specific
circumstances society is willing to pay a hundred or a thousand
times the cost.of the illness  itself  in order to prevent its
occurrence.
   For instance, in general people would be willing to pay more
   than the price of two aspirins to avoid having a headache.

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                              111-66

     More specifically, in the cost-of-illness analyses included
in this report, only the expenses that are directly related to an
individual's medical treatment for the specific symptom being
evaluated at the time the symptom occurs were included.  So, for
instance, no costs are ascribed for the possibility of adverse
effects from the medical treatment or hospitalization itself,
or for the possibility that the specific effect of lead may
precipitate or aggravate other health effects (e.g., children
with anemia are more susceptible to many infections).  Related
expenses, such as the travel costs to obtain medical services
or the costs of making the home environments of children suffering
from lead toxicity safe for them (i.e., altering their diet to
compensate for their propensity to anemia, removing all lead-laden
dust, etc.) were also excluded.  Finally, no value was ascribed
to the pain and suffering of those affected; this  is an especially
significant omission because,  as examples, chelation therapy  is
extremely painful and having a child with lead poisoning or who
is hospitalized can totally disrupt family life.
     We  have also omitted all  the  indirect but related costs  of
lead's adverse effect upon human health.  These  include work  time
lost by  friends and relatives  of the  victims  (including  the
parents  of  lead-poisoned  children); medical  research related  to
the prevention, detection, or  treatment of  the effects of  expo-
sure to  lead;  the development  of new  procedures  to correct the
damage resulting  from lead exposure;  decreased  future  earnings
for  those  suffering  cognitive  damage  (other than very  young

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                               111-67

 children)  or physical  ineapaeitation  (including behavioral dis-
 orders)  from lead's  adverse  effects upon  virtually  every human
 system;  and  the  like.

 III-F.   Summary  of Annual Monetized and Non-monetized
         Children's Health Benefits
     This  chapter presents evidence of a  variety of physiological
 effects  associated with exposure  to lead,  ranging from  relatively
 subtle biochemical changes to  severe  damage and even death at
 very high  levels.  Of  these, only two categories of effects are
 monetized: costs of medical  treatment for  children  with  elevated
 blood-lead levels and  costs  associated with the cognitive  damage
 resulting  from lead's  neurotoxieity.  For  the latter category,
 two alternative monetization techniques were presented:  compensa-
 tory education as a proxy measure and decreased  future earnings
 as as function of IQ points  lost.  In addition,  the numbers  of
 children at risk of several other pathophysiologieal and neurotoxie
 damage each year, including those at  risk  of stature decrements,
 at increased risk of anemia, total number  of children at risk of
 IQ-point-loss, and fetuses exposed to potentially dangerous  lead
 levels, were estimated.  Table III-5  summarizes both the monetized
and non-monetized benefits of reducing exposure to  lead  in drinking
water for one sample year, 1988.

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                                      111-68
TABLE III-5.  Summary of Annual Monetized and Non-monetized Children's
              Health Benefits of Reducing Lead in Drinking Water for
	Sample Year 1988	
Annual Monetized Benefits  (1985 dollars)

   0 Medical costs

   0 Cognitive damage costs:

          compensatory education  (Method 1)
          decreased future earnings  (Method 2)

TOTAL Method 1
      Method 2
 $27.6 million
 $81.2 million
$268.1 million

$108.8 million
$295.7 million
Annual Non-monetized Benefits  (children  at
                                risk of:)

    0  Requiring medical treatment

    0  Loss of 1-2 IQ points
               4 IQ points
               5 IQ points

    0  Requiring compensatory education

    0  Stature decrement

    0  Fetuses at  risk

    0  Increased risk of hematologieal effects
     29,000

    230,000
     11,000
        100

     29,000

     82,000

    680,000

     82,000

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                             CHAPTER IV
        HEALTH BENEFITS OF REDUCING LEAD:  ADULT  ILLNESSES

     Concerns about  the health  effects  of  ambient exposure  to
lead traditionally have focused on  children.  Although  lead has  a
variety of adverse effects on the health of  adults, most  of these
effects were believed to be  a risk  only at high blood-lead  levels.
Recently, many analyses — still the subject of some controversy
— have shown a robust, continuous  relationship between blood
lead levels and blood pressure  in men,  confirming a relationship
between lead exposure and blood pressure that has been  discussed
in the experimental  toxicology  (animal  experiments) literature.
That finding has important implications for the benefits  of
reducing lead in drinking water because high blood pressure, in
turn, is linked to a variety of cardiovascular diseases.
     Other recent human studies show deleterious  effects  of lead
exposure upon fetal and post-natal  growth and development,  both'
mental and physical, that can be correlated with  exposure to lead
in utero.  These studies are discussed  in the previous  chapter on
children's health effects.  In  this  chapter, studies of reproduc-
tive effects on both men and women  are  summarized  briefly,  although
no attempt is made to value these effects monetarily.
     This chapter contains four sections.  Section A discusses the
relationship between body lead  levels and blood pressure  in adult
males,  and includes studies of heart disease as related to  water
hardness.  Section B discusses  some  reproductive  effects of lead
exposure.  Other health effects of  lead, such as kidney function,
immune system function, and hematological effects, are not  discussed

-------
                               IV-2

in this document.  The monetized and non-monetized benefits are
summarized in Section C and some caveats and limitations of this
analysis are found in Section D.
     A more complete discussion of the relationship between lead
and blood pressure is included in the Addendum to the Air Quality
Criteria Document for Lead (U.S. EPA, 1986; appended to Volume 1).
The methods for valuing monetarily the cardiovascular effects
were developed in support of EPA's most recent rule reducing the
amount of lead permitted in leaded gasoline.  These methods are
presented more fully in The Costs and Benefits of Reducing Lead
in Gasoline (U.S. EPA, 1985b).
IV.A.  The Relationship between Blood Lead Levels
       and Blood Pressure
     This section analyzes the statistical relationship between
blood lead and blood pressure.  The  first part provides a brief
overview of human studies relating blood lead levels to blood
pressure and from there links those  changes to cardiovascular
disease rates.  The second part of this section discusses potential
mechanisms and animal data related to lead's effect upon blood
pressure.  The Addendum to the Criteria Document for Lead  (U.S.
EPA, 1986; p.A-1 to A-31) contains a much  fuller analysis  of this
issue and serves as the basis for the summary contained here;  it
also includes a  full bibliography.   The third part of this section
describes studies that have investigated the potential relation-
ship between cardiovascular disease  rates  and water hardness,  and
the possible role of lead in contributing  to cardiovascular disease
when present in  water of different hardness.

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                                IV-3


      While  extremely important,  these findings are still the

 subject  of  some  controversy.   In addition,  these results are

 limited  in  several  ways.   All  of the monetized benefits are

 restricted  to males aged  40  to 59,  because  lead is statistically

 correlated  with  blood pressure only in men,  not women,* and

 because  better data are available for that  age range.   In addi-

 tion, most  of these estimates  cover only  white males,  because  the

 existing studies have had  insufficiently  large samples of non-

 whites.  For these  reasons,  the  cardiovascular health  benefit

 estimates contained in this  section are likely to  understate

 significantly the adult health benefits of  reducing  lead in

 drinking water.  The  most  important omissions  are  older males and

 black males of all  ages.


 IV.A.I.  Epidemiological Studies  of Blood Lead  Levels
         and Hypertension

     Lead has long  been associated  with effects  on blood  pressure

 and the cardiovascular system, including a paper in  the  British

Medical Journal by  Lorimer in  1886  that found that higher blood-

 lead levels increased the risk of hypertension.  Until  recently,

most of the studies focused only on hypertension and relatively

high lead-exposure  levels, and did  not look for  a continuous

effect of lead on blood pressure.  Others failed to find effects

of lead on hypertension that were significant at the 95 percent
   Many fewer studies have investigated the relationship between
   exposure to lead and blood pressure in women.  However, in the
   large-scale general population studies, while blood lead was
   positively correlated with blood pressure in women, it was not
   statistically significant (at the 90 percent confidence level).

-------
                               IV-4

confidence level, although most of them did find a positive
association.  A stronger and
    "more consistent pattern of results has begun to
     emerge from recent investigations of the relation-
     ship between lead exposures and increases in blood
     pressure or hypertension"
     (Addendum to the Criteria Document, p. A-2)
throughout the range of measured blood-lead levels in various
clinically-defined, occupationally-exposed, or general population
groups.
IV.A.I.a.  Occupational Studies
     Kirkby and Gyntelberg  (1985) evaluated the coronary risk
profiles of 96 heavily-exposed lead smelter workers with those of
non-occupationally exposed  workers, matched for age, sex, height,
weight, socioeconomic status, and alcohol  and tobacco consumption.
There were no significant differences  in life style habits, as
far as could be determined.  Diastolic blood pressure was signifi-
cantly elevated among the lead workers, as was the percentage of
lead workers with  ischemic  electrocardiographic  (ECG) changes and
some other  factors.  On the other hand, systolic  blood pressure
and some other cardiovascular risk  factors, e.g., angina pectoris,
were not significantly different.   Overall, the  authors concluded
that long-term lead workers have  higher coronary risk profiles
than a comparable  referent  group  and  that  these  findings may
indicate a  greater risk for major cardiovascular diseases,  such
as myocardial  infarctions or  strokes.

-------
                                IV-5

     Another  study  of  about  50  occupationally-exposed  workers
 (de Kort et al.,  1986)  also  showed blood pressure  levels  to  be
 positively correlated  with blood  lead  levels  at  near or below 60-
 70 ug/dl, after controlling  for confounding variables.

 IV.A.l.b.  Observational Studies
     Moreau et al.   (1982) found  a significant relationship
 (p < 0.001) between  blood lead  levels  and  a continuous measure  of
 blood pressure in 431  French male civil servants after controlling
 for age, body mass  index, smoking, and drinking.   In this  study,
 the correlation was  highest  in  young subjects, and decreased with
 age.  The effect was stronger for systolic pressure than  for
 diastolic pressure  in both the  de Kort and Moreau  studies.  The
 effect was statistically significant in the range  of 12-30 ug/dl
 in the Moreau paper, although the effect was  not large at  that
 level.
     A more recent longitudinal study  by Weiss et al.  (1986)
 examined the blood-lead/blood-pressure relationship in 89 Boston
 policemen.  This study also found a stronger  correlation with
 systolic than diastolic blood pressure.  Weiss' high-lead group
 had blood lead levels >^ 30 ug/dl.
     There are several recent general  population studies, as
well.   Kromhout and Couland (1984) and Kromhout et al.  (1985)
 studied 152 men, aged 57-67,  drawn from the general population.
They found a significant relationship between blood lead and blood
pressure.  However, the statistical significance of the findings
decreased or disappeared after eliminating the highest blood-lead
subject and after multiple regression analyses were conducted

-------
                               IV-6

that included other determinants of blood pressure, such as age
and body mass.  The authors concluded that blood lead is probably
a less important determinant of blood pressure than age or body
mass.
         "The above recent studies provide generally consis-
     tent evidence of increased blood pressure being associat-
     ed with elevated lead body burdens in adults, especially
     as indexed by blood lead levels in various cohorts of
     working men.  None of the individual studies provide
     definitive evidence establishing causal relationships
     between lead exposure and increased blood pressure.
     Nevertheless, they collectively provide considerable
     qualitative evidence indicative of significant associa-
     tions between blood lead and blood pressure levels.
     Particularly striking are the distinct dose-response
     relationship seen for systolic pressure (correcting
     for age, body mass, etc.) by Moreau et al. and the
     findings of significant associations between blood
     lead and systolic pressure after extensive and conserva-
     tive statistical analyses by Weiss et al.  However,
     estimates of quantitative relationships between blood
     lead levels and blood pressure increases derived from
     such study results are subject to much uncertainty, given
     the relatively small sample sizes and limited population
     groups studied.  Two larger-scale recent studies""of general
     population groups, reviewed next, provide better bases
     for estimation of quantitative blood-lead blood-pressure
     relationships."   (Addendum, p. A-10)

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                                IV-7


 IV.A.1.c.   Population Studies

      Pocock et  al.  (1984)  evaluated the  relationships  between

 blood lead  level, hypertension and renal function in a clinical

 study of 7,735  middle-aged (aged  40-49)  British  men.   (This  study,

 conducted by the British government is also called the British

 Regional Heart  Study.)  In that article,  the authors  interpreted

 their findings  as being suggestive of  increased  hypertension at

 elevated blood-lead  levels (>  37  ug/dl),  but not at the lower

 levels  found typically in  British men.   However,  more  recent

 multiple regression  analyses,  adjusted for  variation due to  site,

 reported in  Pocock et al.  (1985)  for the  same data indicate

 highly statistically  significant  associations between  both systolic

 (p =  0.003)  and diastolic  (p <  0.001) blood pressure and blood

 lead  levels.  Noting  the small  magnitude  of the  observed association

 and the difficulty in adjusting for all potentially relevant

 confounders, Pocock et al.  (1985) cautioned  against prematurely

 concluding that there is a causal  relationship between  body  lead

 burden and blood pressure.

     Several other studies of this relationship, discussed below,

have been published using data  from the Second National  Health

Assessment and Nutritional Evaluation Survey  (NHANES II),* which

provide careful blood lead and  blood pressure measurements on a
   The NHANES II was a 10,000 person representative sample of the
   U.S. non-institutionalized population, aged 6 months to 74
   years.  The survey was conducted by the (U.S.) National Center
   for Health Statistics (NCHS) ~over a four-year period (1976-1980)
   The data base is available from NCHS and analyses of the lead-
   related data from it have been published before (e.g., Annest
   et al., 1982 and 1983; Mahaffey et al., 1982a and 1982b; Pirkle
   and Annest, 1984) .

-------
                               IV-8





large-scale sample representative of the U.S. population and



considerable information on a wide variety of potentially confound-



ing variables, as well.  The studies using the NHANES II data



avoided the problems of selection bias, healthy worker effect,



work place exposures to other toxic agents, and appropriate choice



of controls, that had complicated or confounded many of the other



studies (cf, Addendum to the Criteria Document, 1986; p. A-12ff).



     Simple correlation analyses reported by Harlan et al. (1985)



demonstrated statistically significant linear associations



(p < 0.001) between blood lead concentrations and blood pressure



(both diastolic and systolic) among males and females, aged 12-74



years.  Controlling for many potentially confounding factors,



multiple regression analyses showed the blood-lead/blood-pressure



relationships remained significant for males but not for females.



     Pirkle et al.  (1985) conducted additional analyses on the  '



NHANES II data.  That  study  focused on white males, aged 40-59,



to avoid the effects of collinearity with age, and because of less



extensive NHANES II data being available for non-whites.  In  the



subgroup studied, Pirkle et  al.  found significant associations



between blood lead  levels and blood pressure both in basic models



and after including all the  known  factors previously established



as being correlated with blood pressure.  The  relationship also



held, with  little change in  the  coefficient, when tested against



every dietary and serological variable measured  in the  NHANES II.



           "No evident  threshold  was found below  which blood



      lead  level  was not significantly  related  to blood  pres-



      sure across  a  range of  7 to 34 ug/dl.   The  dose-response

-------
                           IV-9



 relationships characterized by Pirkle indicate that

 large initial increments in blood pressure occur at

 relatively low blood-lead levels, followed by a leveling

 off of blood pressure increments at higher blood-lead

 levels.   Pirkle et al.  also found lead to be a signifi-

 cant predictor of diastolic blood pressure greater than

 or equal to 90 millimeters of mercury (mm Hg),* the

 criterion blood pressure level now commonly employed in

 the United States to define hypertension.   Additional

 analyses were performed by Pirkle et al.  to estimate the

 likely public health implications of the  Pirkle findings

 concerning the blood-lead/blood-pressure  relationship.

 Changes  in blood pressure  that might result from a speci-

 fied  change  in blood lead  levels  were first estimated.

 Then  coefficients from  the  Pooling Project and  Framingham

 studies  (Pooling Project Research Group,  1978;  and McGee

 and Gordon,  1976,  respectively)** of cardiovascular disease

 were  used  as  bases:   (1) to  estimate the risk for  incidence

 of  serious cardiovascular events  (myocardial infarction,

 stroke, or death)  as a  consequence  of  lead-induced  blood

 pressure  increases and  (2) to predict  the  change  in the

 number of serious outcomes as the  result of a 37 percent

 decrease  In blood lead  levels for  adult white males  (aged

 40-59 years) observed during the  course of the NHANES II

 survey (1976-1980).."'  (Addendum, p. A-13).
*   Millimeters of mercury is the standard measure of blood
    pressure.


**  These are discussed more fully in Section IV.A.4., below.

-------
                              IV-10

Schwartz (1985) expanded the Pirkle et al. analysis to include
all men over 20, and examined the 20-44 and 45-74 age groups
separately.  In all three groups, lead was significant both in
basic models and when tested against the much-larger variable
list.  Schwartz also showed that lead was significant even with
the inclusion of a linear time-trend term.
        "Questions have been raised by Gartside  (1985) and
     Du Pont (1986) regarding the robustness of  the findings
     derived from the analyses of the NHANES II  data as to
     whether certain time trends in the NHANES II data set
     may have  contributed to  (or account  for) the reported
     blood-lead/blood-pressure relationships...
     However,  neither the Gartside nor the Du Pont analyses
     adjusted  for all of the variables that were selected
     for stepwise inclusion  in the Harlan et al. (1985) and
     Pirkle et al.  (1985) published studies."   (Addendum, p.  A-14)
Reanalyses of  the NHANES II  data by Schwartz  (1986)  showed  that
lead remained  a significant  factor even  if a linear  time  trend
was  included  in the  regression,  and also remained  significant in
regressions that adjusted for all  of  the sites  visited  in NHANES
II,  which  controls  for  both  time  (the sites were visited  sequenti-
ally)  and  geographical  variation.  Schwartz  also showed that  the
relationship  held in all  adult men,  in men under 45, and  in men
over 45, as well as  in  the  age group  of  Pirkle  et al.   These
reanalyses were reviewed  and accepted by EPA's  external Science
Advisory Board.

-------
                             IV-11



          "In order to more definitively assess the robust-


      ness of the Harlan et al.  (1985)  findings and, also,


      to evaluate possible  time-trend effects  confounded by


      variations  in sampling sites,  Landis  and Flegal (1986)


      carried out further analyses for  NHANES  II  males,  aged


      12-74,  using a randomization model-based approach  to


      test  the  statistical  significance of  the partial cor-


      relation  between blood lead  and diastolic blood pres-


      sure, adjusting  for age, body  mass  index, and  the  64


      NHANES  II sampling  sites.  The resulting analyses  con-


      firm  that the  significant  association between  blood lead


      and blood pressure  cannot  be dismissed as spurious due


      to concurrent  secular  trends in the two  variables over


      the NHANES  study period."  (Addendum, p. A-14)


      in addition, EPA has conducted a  series  of additional reanaly-


ses of the NHANES II data to address the issue of "site" more


definitively.


         "These unpublished analyses* confirm that the regres-


     sion coefficients remain significant for both systolic


     and diastolic blood pressure when site is included  as  a


     variable in multiple regression analyses."  (Addendum,

     p.  A-15)
         ™           Central  ^cket  Section  of  EPA.   Docket  number,
        -CD-81-2;  documents numbered IIA.F.60,  IIA.C.5,  II.A.C  9
    and  IIA.C.11.                                                '

-------
                         IV-12





    "Overall, the analyses of data from the two large-



scale general population studies (British Regional Heart



Study and U.S. NHANES II study), conducted both in this



country and in Great Britain, collectively provide



highly convincing evidence demonstrating small but



statistically significant associations between blood



lead levels and increased blood pressure in adult men.



The strongest associations appear to exist for males



aged 40-59 and for systolic pressure somewhat more than



for diastolic.  Virtually all of the analyses revealed



positive associations for the 40-59 age group, which



remain or become significant  (at p < 0.05) when adjust-



ments are made for geographic site.  Furthermore, the



results of these large-scale  studies are consistent with



similar findings of  statistically significant associations



between blood lead levels and blood pressure  increases



as  derived from other recent  smaller-scale studies dis-



cussed earlier, which also mainly found stronger  associa-



tions  for  systolic pressure  than  for diastolic.   None  of



the observational studies  in  and  of themselves  can be



stated as  definitively  establishing causal  linkages



between  lead exposure and  increased blood  pressure or



hypertension.  However, the plausibility  of  the observed



associations reflecting causal  relationships  between



 lead exposure and  blood pressure  increases is supported



by:  (1)  the consistency of the significant  associa-



 tions that have  now been found by numerous independent

-------
                          IV-13





 investigators for a variety of study populations; and



 (2) by extensive toxicological data (see below) which



 clearly demonstrate increases in blood pressure for



 animal models under well-controlled experimental con-



 ditions.  The precise mechanisms underlying the relation-



 ships between lead exposure and increased blood pressure,



 however, appear to be complex, and mathematical models



 describing the relationships still remain to be more



 definitively characterized.  At present,  log blood-lead/



 blood-pressure (log PbB-BP) models appear to fit best



 the available data,,  but linear relationships between



 blood lead and blood pressure  cannot be ruled out at



 this time.   The  most appropriate  coefficients charac-



 terizing blood-lead/blood-pressure relationships also



 remain to be more  precisely determined,  although those



 reported by  Landis  and  Flegal  (1986) and  those obtained



 by  analyses  adjusting for site appear to  be  the currently



 best available and most reasonable  estimates  of the



 likely strength  of  the  association  (i.e., generally  in



 the  range of  2.0-5.0 for log PbB versus systolic and  1.4



 to  2.7  for log PbB versus diastolic blood pressure)."



     "Blood lead  levels  that may be  associated  with



 increased blood  pressure also  remain to be more  clearly



defined.  However, the  collective evidence from  the



above  studies points toward moderately elevated  blood-



lead levels  (>_ 30 ug/dl) as being associated most clearly



with blood pressure increases, but  certain evidence

-------
                         IV-14

(e.g., the NHANES II data analyses and the Moreau
et al. study results) also indicates significant (and
apparently stronger) relationships between blood pressure
elevations and still lower blood lead levels that range,
possibly, to as low as 7 ug/dl.  This may be supported
by several animal studies, discussed below, that also
find hypertension most consistently related to relatively
low exposure levels but over  relatively long exposure
periods."
    "The quantification of likely consequent risks for
serious  cardiovascular outcomes, as attempted by Pirkle
et al.  (1985), also  remains to be more precisely charac-
terized.  The specific magnitudes of  risk  obtained for
serious  cardiovascular outcomes  in  relation to  lead
exposure, estimated  on the  basis of lead-induced blood
pressure increases,  depend  crucially  upon:  the  form of
the underlying  relationship and  size  of  the coefficients
estimated for blood-lead/blood-pressure  associations;
 lead  exposure  levels at  which significant elevations in
blood pressure  occur?  and coefficients  estimating  rela-
 tionships between blood  pressure increases and specific,
more-serious cardiovascular outcomes.  As noted above,
 uncertainty still exists regarding the most appropriate
 model and blood-lead/blood-pressure coefficients,  which
 makes it difficult to resolve which specific coefficients
 should be used in attempting to project more serious
 cardiovascular outcomes.  Similarly, it is difficult to

-------
                               IV-15

      determine appropriate blood-lead levels at which any
      selected coefficients might be appropriately applied in
      models predicting more serious cardiovascular outcomes.
      Lastly, the selection of appropriate models and coeffi-
      cients relating blood pressure increases to more serious
      outcomes is also fraught with uncertainty...
      Further analyses of additional large-scale epidemiologic
      data  sets may be necessary  in order to determine more
      precisely quantitative relationships between blood lead
      levels and blood pressure,  and more serious cardiovascu-
      lar outcomes as well."
         "The findings discussed here, while pointing toward
      a  likely causal effect  of lead in contributing  to increased
      blood  pressure,  need  to be  placed in broader perspective
      in relation to  other  factors involved in the etiology of
      hypertension.   The  underlying  causes of increased blood
      pressure or "hypertension"  (diastolic blood pressure
      above  90  mm Hg),  which  occurs  in as  many as 25 percent
      of Americans, are not yet fully delineated.   However,
      it is  very  clear  that many  factors contribute to  develop-
     ment of  this disease, including hereditary  traits,
      nutritional  factors and environmental  agents."   (Addendum,
     p. A-15  to A-18)
     The contribution of lead, compared to many  other  factors
such as age, body mass, and smoking, appears  to  be relatively
small, but  the findings have stayed robust  in the face of repeated
reanalyses  and specifications of the models.

-------
                              IV-16


IV.A.2.  Mechanisms Potentially Underlying Lead-Induced
         Hypertension Effects

         "This section [briefly summarizes] .plausible bio-

     chemical-physiological mechanisms by which lead poten-

     tially influences the cardiovascular system to induce

     increased blood pressure, followed by  [a short discussion]

     of experimental evidence concerning the contribution of

     lead exposure to the development of hypertension.

          "Blood pressure is determined by  the  interaction

     of two factors:  cardiac output and total  peripheral

     resistance.   An elevation of  either or both results  in

     an  increase  in blood pressure.  A  subsequent  defect  in  a

     critical regulatory function  (e.g.,  renal  excretory

     function)  may influence central nervous  system regulation

     of  blood pressure,  leading  to a permanent  alteration in

     vascular smooth muscle tone which  sustains blood pressure

     elevation.  The primary defect in  the pathophysiology of

      hypertension is thought to be due  to alteration in cal-

      cium binding to plasma membranes  of cells; this change

      in calcium handling may in turn be dependent upon an

      alteration in sodium permeability of  the membrane (e.g.,

      Hilton, 1986).  This change  affects several pathways

      capable of elevating pressure:  one  is a direct altera-

      tion of the  sensitivity of vascular  smooth muscle to

      vasoactive stimuli? another  is indirect,  via  alteration

       of neuroendocrine input to vascular  smooth muscle  (includ-

       ing changes  in renin  secretion rate)."  (Addendum,  p.  A-18)

-------
                              IV-17

IV.A.2.a.  Role of Disturbances in Ion Transport
           by Plasma Membranes
         "Many stimuli activate target cells in the mammalian
     body via changes in ion permeabilities of the plasma
     membrane, primarily for sodium,  potassium, and calcium
     ions;  the change in calcium ion  concentration is the
     primary intracellular signal controlling muscle contrac-
     tions,  hormone secretion, and other diverse activities...
     For  calcium,  there  is a membrane potential-dependent
     sodium/calcium exchange pump which extrudes one calcium
     ion  in  exchange for three sodium ions.   In addition,
     there are calcium ATPase pumps located  at cell  membranes
     and  at  intracellular membrane storage  sites (endoplasmic
     reticulum and  mitochondria)...   The  ion interacts with
     several  calcium-binding proteins which,  in turn, activate
     cell contractile  or  secretory processes.
         "It  has been  postulated  that sodium pump  inhibition
     by some  endogenous factor  (thought to be  a  hormone)
     would be  ultimately  causatory for development of both
     essential  and volume-expanded hypertension  by affecting
     vascular  tone or  resistance.
        "If  lead exposure could be shown to affect sodium
     transport  (which, then,  indirectly alters vascular
     resistance) or to directly affect vascular resistance
     (by changing calcium ion permeability or transport), it
    could contribute to the development of hypertension...

-------
                              IV-18

    Abundant experimental  evidence...  indicates  that
    lead  affects  both;  that is, lead inhibits  cell  membrane-
    bound sodium-potassium-ATPase as well as interferes with
    normal processes of calcium transport across membranes
    of various tissue types...  Lead acts to alter  sodium
    balance and calcium-activated cell activities of
    vascular smooth muscle.  Changes in either or both of
     these could be expected to produce changes in blood
     pressure regulation."   (Addendum, p. A-18 to A-19)

IV.A.2.b.   Role of Renin-Angiotensin in Control of Blood Pressure
           and Fluid Balance
     One major endogenous factor regulating total peripheral
resistance of the vascular smooth muscle  is angiotensin II (AII)f
a small peptide generated in plasma via the action of a renal
hormone, renin.
         "The renin-angiotensin system has a major  influence
     on regulation of blood pressure,  [both directly and
     indirectly.  It directly affects vascular smooth muscles
     to increase  vasoconstriction and  it  indirectly  increases
     total peripheral resistance by  affecting  the discharge
     rate  of sympathetic neurons.]   For  this reason, investi-
     gators  interested  in hypertension have  studied the
     system in detail.  Because renal  disease  may be an
     important initiating  event in  subsequent  development of
     hypertension and because lead  is  an important  renal
     toxicant,  some  investigative reports of patients  with
     lead intoxication have evaluated blood pressure changes

-------
                               IV-19

      and  changes  in  the  renin-angiotensin system."   (Addendum,
      p. A-20  to A-21)
      However, the  results of  these studies  have  been  contradictory.
The few human studies have  shown  depressed,  increased and  unaltered
renin activity in  lead intoxicated men.   The studies  may not be
comparable because some used men  with chronic sub-clinical lead
exposure as compared to chronic heavy lead exposure,  and some
subjects had exposure which would be considered  "normal".
     In addition,  there have been animal  and experimental studies,
investigating the cardiovascular effects  of both acute and chronic
exposure to lead.
         "Lead injected intravenously in dogs and rats, at
     doses as low  as  0.1  mg/kg (whole blood lead < 5 ug/dl
     and renal lead of  1.2  ug/g)  produced over the next
     several  hours significant increases in plasma renin
     activity (PRA) and  in  excretion  of  sodium,  other  cations,
     and water (Mouw  et al., 1978)...  The increased sodium
    excretion could  be attributed to decreased  sodium reabsorp-
    tion.  The mechanism of lead's action on  tubular  reabsorp-
    tion was  not  determined,... nor was  the mechanism by which
    lead  increased renin secretion.
        "In a subsequent study, Goldman  et al.  (1981)  found
    that the rise  in PRA after acute lead injection was not due
    to increased renin secretion  in six  of nine  dogs;  rather
    there was elimination of hepatic renin clearance,  without
    evidence for other interference in liver function.  in
    the remaining three dogs, renin secretion increased; this
    was thought to be due to lead activation of normal mechanisms

-------
                         IV-20





for renin secretion, although none of the classic



pathways for influencing renin secretion were altered.



The authors postulated that lead might produce altera-



tions in cytosolic calcium concentration in renin-



secreting cells...  The authors also postulate that



there may be multiple actions of lead on the renin-angio-



tensin system which may help explain confusion about  the



ability of lead to cause hypertension.  At certain



exposure conditions, there  could be elevated PRA without



simultaneous inhibition of  angiotensin-converting enzyme,



thereby contributing to hypertension, while higher  doses



or  longer exposure might  inhibit the converting enzyme



and thereby  cause loss of  hypertension...



     "The literature of experimental  findings  of  lead-



 induced  changes  in the  renin-angiotensin system and



 blood pressure  in animals  is  complicated by  apparently



 inconsistent results  when comparing one study to another.



 All studies  report changes in the  renin-angiotensin



 system,  yet  some studies fail to find an effect on blood



 pressure and others do report hypertension.   Doses and



 exposure periods employed vary widely,  but in general,



 hypertension is observed most consistently with relative-



 ly low doses over relatively long exposure periods...



     "Perry and Erlanger (1978) found that chronically



 feeding rats either cadmium or lead at doses of 0.1,



 1.0, or 5.0 parts per million (ppm) produces statistically



 significant increases in systolic blood pressure...

-------
                          IV-21





 The implications for human populations exposed to very



 low doses of these metals were pointed out.  Victery et



 al. (1982a) reinvestigated the question, using lead



 doses of 100 and 500 ppm administered in the drinking



 water to rats beginning while the animals were in utero



 and continuing through six months of age.  At 3-1/2



 months of age, the male rats drinking 100 ppm of lead



 first demonstrated a statistically significant increase



 in systolic blood pressure;  this difference persisted



 for the remainder of the experiment.  Animals drinking



 500 ppm had lower pressures,  which were not significantly



 different from controls.   Female rats drinking 100  ppm



 did not demonstrate pressure  changes.  At termination of



 the experiment  PRA  was  significantly decreased by 100



 ppm lead exposure,  but  not 500 ppm...  There was  a



 dose-dependent  decrease in the ratio of  [angiotensin  II



 to  plasma renin activity] for lead-exposed  rats.  Renal



 renin was  depressed  in  lead-exposed  animals.   The hyper-



 tension  observed  in  these animals was not secondary to



 overt renal disease  (as opposed to an effect  on renal



 cell metabolism), as evidenced by a  lack of  changes in



 renal histology and plasma creatinine.



    "Victery et al.  (1983) examined  changes  in the renin-



angiotensin system of rats exposed to lead doses of 5,



25, 100, or 500 ppm during gestation  until one month of



age.  All had elevated plasma renin activity, while



those at 100 and 500 ppm also had increased renal renin

-------
                              IV-2 2

     concentration.  Lead-exposed animals...  secreted
     less  renin  than control  animals.   It  appears  that  lead
     has two  chronic effects  on  renin  secretion, one  inhibi-
     tory  and one  stimulatory; the magnitude  of effect  on PRA
     reflects the  dose and timing of the lead exposure  as
     well  as  the physiological state of the animal.
        "In  another study, Victery  at al. (1982b) reported
     that  rats fed 5 or 25 ppm lead  for five  months  (blood
     lead  of  5.6 and 18.2 ug/dl, respectively) did not  develop
     hypertension  but  at 25 ppm  had  significantly  decreased
     PRA.   Both groups of animals  had  a decrease  in the All
     to PRA ratio.  Thus, lead exposure at levels  generally
     present  in the human population caused observable  effects
     in renin synthesis." (Addendum, p. A-23 to A-25)

IV.A.2.C.   Effects of  Lead on Vascular Reactivity
         "Piccinini et al. (1977)  and Favalli et al. (1977)
     studied the effects of lead on calcium exchanges in the
     isolated rat tail artery;  lead in concentrations of up
     to 15 umol in. vitro produced contractions which required
     the presence of calcium  in the perfusion solution.
     Therefore, calcium  influx was not affected by lead...
     Tissue  calcium content was increased...
          "Tail  arteries  obtained from  the  hypertensive rats
     in the  study performed by  Victery et al. showed an
     increased  maximal contractile  force  when tested in  vitro
     with the alpha-adrenergic  agents  norepinephrine and

-------
                               IV-2 3
      methoxamine (Webb et al., 1981).  This finding is apparently
      related to an increase in the intracellular pool of activator
      calcium in the smooth muscle cells in the artery.  This
      change may also be responsible for decreased relaxation
      of the muscle after induced contractions.
          "rn vivo tests of cardiovascular reactivity in rats
      exposed to 50  ppm lead (blood lead 38.4  + ug/dl)  for 160
      days were  performed by lannaccone et al.  (1981).   [This
      study showed]  significant increases in systolic and  diastolic
      pressure  [related to lead exposure,  as well  as  significant
      increases  in the  blood  pressure  response  to  noradrenalin].
      The  data suggest  that  the lead-related increase in arterial
      pressure is due at  least  in part  to greater  sympathetic
      tone, with the metal affecting neural control of  blood
     pressure." (Addendum, p. A-26 to A-27)

IV.A.2.d.  Effects of Lead on Cardiac Muscle
     Lead has been hypothesized to contribute to cardiomyopathy
and to have cardiotoxic properties.
         "Kopp et al. (1978) developed an in vitro system for
     monitoring the cardiac electrical conduction system
     (electrocardiogram or EGG) and systolic tension, and
     demonstrated that  _in vitro lead (3 x 10-2 mM) or cadmium
     (3  x 10-2 mM)  depressed systolic  tension  and  prolonged the
     P-R interval  of the EGG...  [in a later study,]  hearts
     obtained from rats exposed to  low levels  of cadmium and/or
     lead  (5  ppm)  for 20  months were found  to  have... changes
     in  the heart's  electrical  conduction  system (Kopp  et  al.,
     1980)  with  significant  prolongation of the  P-R interval...

-------
                         IV-2 4

     "Williams et al. (1983) suggested that much of the
negative effect of lead on cardiac tissue and ECG abnor-
malities can be related to lead's interference with
calcium ion availability and/or membrane translocation.
In addition, even those lead exposure-related effects
that appear to occur through autonomic nerves may be
understood in terms of effects on calcium ion, which  is
required for neurotransmitter release...
    "Prentice and Kopp (1985) examined functional and
metabolic responses of the perfused  rat heart produced
by lead with varying calcium concentrations  in the  per-
fusate.  Lead altered the spontaneous contractile
activity, spontaneous electrical  properties  and  metabo-
lism of the heart tissue.   The exact mechanisms  were  not
completely  resolved  but  did involve  disturbances in cellu-
lar calcium metabolism,  although  not by  any  single
mechanistic model...
     "In addition,  hearts perfused with  30  uM lead had
reduced coronary blood  flow, presumably by lead  acting
to directly constrict the vascular smooth muscle or by
 interference with the local metabolic stimuli for vaso-
 dilatation.  Increases in perfusate calcium concentration
 partially reversed this effect,  although at the highest
 calcium levels (5.0 mM)  coronary blood flow was again
 reduced.  These authors concluded that their present
 findings were consistent with those of others which

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                              IV-25


     showed increased vascular reactivity and that the

     chronic lead exposure-related changes in blood pressure

     may be related to localized actions of lead on vascular

     beds and arterial smooth muscle." (Addendum, p. A-27 to

     A-29)


IV.A.2.e.  Summary of Lead-Related Effects
           on the Cardiovascular System

         "Blood pressure is regulated and affected by many

     interactive forces and control systems;  some of these

     have been shown to be affected by lead  exposure.   Under-

     standing of the effects of  lead on each system is still

     preliminary,  but sufficient  evidence indicates that

     changes  which occur in the presence  of  lead can promote

     the  development of  hypertension...   Although the

     exact mechanisms involved in lead-induced  changes in

     renin secretion rate  have not  been examined,  it  is

     likely that lead  could be affecting  the cystosolic  free

     calcium ion of  [some]  cells...  After lead  enters

     [these] cells,  lead could enhance or block  calcium  exit

     via  sodium/calcium exchange  pumps, or increase or

     decrease the  intracellular sequestration of calcium in

     storage compartments...

         "The changes  in vascular reactivity which have  been

     reported in animals chronically exposed to  lead are

    probably the key finding which can lead to  an under-

    standing of how lead can contribute to the  development

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                              IV-2 6


    of hypertension.  The vascular  smooth muscle  changes

    are necessary  and sufficient in themselves  to account

    for the  increase  in  blood pressure  and  the  fact  that

    these  changes  are observed in animals exposed to rela-

    tively low lead levels  makes  it increasingly  important

    to evaluate these findings in additional experimental

    studies.   There may  be  additional changes in  the entire

    sympathetic neural control of vascular  tone which acts

    to  amplify the contractile response to  any endogenous

    vasoconstrictor substance." (Addendum,  p. A-29 to A-30)


IV.A.3.   Cardiovascular  Disease Rates and Water Hardness

     Since Kobayashi's study  (1957)  was highlighted by Schroeder

(1958),  studies in several countries have evaluated the relation-

ship between drinking water characteristics and death from

hypertensive, ischemic or arteriosclerotic heart  diseases,

and in particular the relationship  between cardiovascular disease

(CVD)  rates and water hardness.*  Generally,  the  studies covering

large geographic regions have  shown a significant inverse rela-

tionship between the hardness of local  drinking water and local

CVD rates.  However, not all  the studies, most  commonly not the

studies involving  smaller geographic regions, evidence the  same

consistency of  effect.
 *  Water hardness  is  determined  by  the  relative  amount  of  dissolved
   solids,  primarily  calcium and magnesium,  in it.   It  is  expressed
   as  the equivalent  amount of calcium  carbonate (CaC03) that could
   be  formed from  the calcium and magnesium  in solution.   For a_
   fuller discussion  of  this issue, see Chapters II  and V_of this
   document.  Generally, water  < 60 mg/1 as  CaC03 is considered
    'soft1.   Most studies investigating  CVD and water hardness have
   focused  upon systems  with very soft  water,  i.e.,  < 40 mg/1 as

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                               IV-2 7

      The U.S. National Research Council, of the National Academy
 of Sciences, convened a panel of experts in the late 1970s to
 review this issue.  The panel concluded that the findings were
 "strikingly" equivocal and called for additional research (Angino,
 1979).   Since then, many additional reviews have attempted to
 resolve the inconsistencies in the data; none has succeeded.   Two
 noteworthy reviews (Comstock, 1979;  Comstock, 1985)  apply rigorous
 statistical and epidemiologic tests  to the literature on the
 relationship between water hardness  and CVD.   This section contains
 a  very  brief survey of the nature of these studies,  plus a suggest-
 ed explanation for the inconsistent  findings.

 IV.A.3.a.   Studies of Cardiovascular Disease  and Water Hardness
      The  largest category  of  studies is the intra-national studies,
 where various  population units within several  different countries
 were  examined.   Generally,  these  studies have  found  a statistically
 significant  inverse  relationship  between CVD  and water  hardness,
 and account  for  the  phrase:   'soft water, hard arteries1.
     A second category of  studies —  geographic  units comprising
 states or provinces  — in  general show  a similar but  weaker
 negative association between CVD mortality  and water  hardness.
     Studies of  selected communities  that are not in  the same
geographic unit and that have different water hardnesses have
been least likely to show consistent  findings linking CVD and
water parameters; the inconsistencies of findings have included
associations with water hardness that were  in opposite directions
for the  two sexes or for different categories of cardiovascular
illnesses, as well as statistically insignificant associations.

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                              IV-2 8

     Fewer of the studies conducted in the past decade have found
the significant negative associations that were found in some of the
e'arlier papers.
     Ipterest in identifying a 'water factor1 that influences heart
disease has continued because CVD rates vary significantly by
geographic regions (Sauer, 1980).  Water parameters also tend to
portray regional patterns and, therefore, could offer a tenable
explanation for the geographic variation in mortality.  Further,
water treatment costs are lower  than medical treatment costs.*  At
the water system level, reducing  the presence of a harmful sub-
stance or correcting the deficiency of a protective one is both
relatively easily done  and effective in reaching large numbers of
people.
     There are many plausible mechanisms for recognizing an  effect
from the constituents and parameters of water upon heart disease.
The presence  or  selective absence of trace  elements are the  most
likely sources of an effect  on health  related  to corrosive water.
Or soft water may initiate heart disease,  or soft water parameters
added onto  other factors  that predispose  a person to  heart disease
may be sufficient to push him/her over the threshold  to  symptomatic
 illness,  or it may  exacerbate  a  pre-existing condition,  either
 recognizable or  asymptomatic.   Soft water may  contain harmful
 contaminants or  hard  water  may  contain protective  elements lacking
 in soft  water.   Most  probably,  some combination of  these  scenarios
 accounts for the association.
 *  For instance, treatment to increase water hardness costs
    $1-2 per person per year as opposed to one heart attack,
    which costs $65,000 per case.

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                               IV-2 9

     Generally,  there  are  three  broad  classes  of mechanisms  by
which water can  be postulated  to affect CVD  in either  a  causative
or detrimental manner.
D  Soft water is deficient in some major cations that are protec-
    tive to the  cardiovascular system  and that are abundant  in
    hard water.  The most  likely of these are  calcium and magne-
    sium, which  are the major components of  hardness in  water.
    Some epidemiological studies (e.g., Abu-Zeid, 1979;  though
    not all, e.g., Miller  et al., 1985) have shown magnesium to
    be a strong  factor in  cardiovascular health.
2)  Protection of the cardiovascular system by specific minor
    cations or trace metals that are more abundant in hard water
    than soft water.   Of these,  lithium, chromium, manganese,
    selenium,  vanadium, and strontium are possible contributors.
    All, with the possible exception of vanadium, are essential
    micronutrients and could have plausible involvement with CVD
    rates.
3)  Soft water leaches toxic metals  from the distribution system.
    Studies relating  water hardness  to CVD have considered
    especially three  potential toxins:   cadmium,  copper,  and
    lead.   Copper is  perceived as the  least likely of the three,
    and  strong evidence exists linking both lead  and  cadmium to
    hypertension.  All three metals  are corrosion by-products.
    (It  is  interesting, in this light,  to  note  that water is a
    more significant  source of lead  in Britain  than the U.S.  and
    the  hard-water/CVD association appears  more robust  there.)

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                               IV-30

     Overall, the two constituents most seriously considered in
current analyses are the protective role of magnesium (less
common in soft water than in hard water) and a detrimental effect
from increased sodium (which is often added in water softening
units).*
IV.A.S.b.  Lead, Soft Water and Cardiovascular Disease
     While the geographic variation in CVD probably relates to
several factors and the interrelationships between them, the new
studies relating blood lead levels to blood pressure could help
resolve some of the inconsistent  correlations between cardiovascular
disease and  soft drinking water.  Lead occurs in drinking water
as a corrosion by-product, that is, as a result of the  action of
corrosive water upon  the materials  (pipes  and particularly solder)
of the distribution and residential plumbing systems.** Hardness/
softness of  water  is  one measure  of a water's potential corrosivity,
but because  water  chemistry  is very complicated, no  single measure
is an  adequate  predictor of  a  specific  water's  actual  corrosivity
or of  the presence of corrosion by-products,  including  lead  (cf,
for  instance, Patterson,  1981).
      Relatively few of the  studies investigating  the relationship
between water hardness and  CVD rates  have  considered the presence
 *   It has been suggested that the relatively recent increase in
     sodium intake in populations in hard water areas may be negating
     the advantages once associated with those hard water areas
     (Comstock, 1985).
 **  For a fuller discussion of these studies, see Section II.A.,
     above, or Section V.A., below.

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                               IV-31


 of  trace metals  at  all  (e.g.,  Sharrett  et  al.,  1984)  or the  water

 sampling procedures have  not addressed  the occurrence phenomena

 of  corrosion by-products.*  Often, the  water data  represent  lead

 levels  in the distribution  system  (e.g., Shaper et al.,  1980;  or

 Craun and McCabe, 1975, which  uses data from the 1969 Community

 System  Survey, presented  in McCabe et al.,  1970);  or  tap water

 typical of the distribution system- (i.e. ,  fully flushed);  or tap

 water averaged with distribution system water (e.g.,  Greathouse

 and Craun, 1978; or Greathouse and Osborne,  1980;  which  use  data

 from the First National Health and Nutrition Augmentation  Survey,

 in which one random daytime tap sample  was  averaged with 12

 monthly samples  from the water supply).

     In the few  studies that did consider  exposure to corrosion

 by-products, other  problems have arisen.   In Calabrese and Tuthill

 (1978), for instance, the lead levels in the two communities

 studied were not statistically significantly different.  Other

 studies have not withstood  rigorous statistical  testing  (e.g.,

 Hewitt and Neri, 1980).

     Considering the data linking blood pressure (and CVD) to

 exposure to lead, the studies  correlating CVD with water hardness

may be imperfectly measuring the relationship between soft drinking

water and the presence of lead (and/or cadmium).  In other words,

 the studies that have found a  relationship between soft water and

heart disease may actually have evaluated systems with higher-than-
*  That is, contamination of drinking water that occurs due to
   the corrosive action of the water upon the materials of the
   plumbing systems.  Several of the trace constituents of concern,
   including lead, copper and cadmium, are corrosion by-products.
   This issue is discussed in Chapter II of this document.

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                              IV-3 2


average lead levels, resulting from softer water leaching more lead

from the plumbing.  However, while softer water is more likely

to contain higher lead (or cadmium) levels, the factors related

to lead contamination are very complicated.  Soft water alone is

not predictor of lead levels, and therefore, not all systems with

soft water have higher metals.  This may account for some of

the inconsistent findings.

     Another factor is that the major elements of hard water are

magnesium and calcium which can be easily absorbed in the small

intestine and therefore may compete with lead for some common

transport system or metabolic interactions, as explained by

Conrad and Barton (1978) and Mahaffey and Rader  (1980).  The

relationship between calcium intake and  lead absorption  is not

yet clear.  Some early studies  (e.g., Aub,  1935)  indicated that

increased calcium intake could  reduce blood lead  levels; other

studies have shown more complicated relationships between calcium

intake and  lead absorption  and  retention,  including  lead's effect

upon calcium metabolism  (Six and  Goyer,  1970 and  1972; Quarterman

et al., 1978; also  cf  the discussions on lead  and calcium  in  both

the Criteria Document, 1986, p.  10-44 to 10-48,  and  its  Addendum,

p. A-18ff).


IV.A.4  Benefits  of Reduced Cardiovascular Disease;   Reductions
        in  Hypertension  and Related Morbidity  and Mortality

     On the basis of  the  data discussed  above  on the association

between lead body burden and increased  blood pressure in adult

males,  this analysis  assumes that reducing lead  in  drinking  water

could  reduce blood  lead  levels, which in turn  could reduce blood

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                               IV-3 3

 pressure  and  the  number of individuals with hypertension.   A
 reduction in  hypertension  would  have  direct benefits from  reduced-
 medical treatment expenditures.  More important,  however,  are
 the  related benefits  in the  form of reduced cardiovascular disease
 associated with elevated blood pressure.   This  section  describes
 the  methods used  to estimate the benefits  associated with  lowering
 blood pressure, including  estimating  the reductions  in  morbidity
 and  mortality.
     Estimating the reduction in hypertension and  cardiovascular
 disease requires  several steps.  The  first is to  estimate  the
 impact of the reduction of lead  levels  in  drinking water on
 levels of lead in adults'  blood.  For that,  the occurrence data
 and  water-lead to blood-lead equations  described  in  Chapter II
 were combined with the  regression analyses of the  NHANES II  data
 discussed previously.   In  each ease,  the blood lead  levels in the
 NHANES II data were first  adjusted to reflect reductions in
 environmental lead contamination that have occurred  since  the
 time of the survey.
     To calculate  the cardiovascular  benefits, logistic regression
 equations were used to  predict how reducing exposure  to lead in
 drinking water could affect  the number  of  hypertensives in  the U.S.
 population.  These estimates  cover only males aged 40 to 59,
 because the effect of lead on blood pressure appears  to be  stronger
 for men and because the  correlation between blood pressure  and
 age  is much smaller in this age range,  reducing the potential
 for confounding due to the correlation  between blood  lead  and
age.   The  estimates of reduced cases of cardiovascular and

-------
                              IV-3 4


cerebrovascular disease rely upon (1) site-adjusted coefficients

from analyses of the NHANES II data relating blood lead levels to

increases in blood pressure* and (2) coefficients relating blood

pressure increases to more serious cardiovascular disease outcomes,

based on data from the Framingham Study and Pooling Project (1976),

discussed below.

     The estimates of myocardial infarctions, strokes and deaths

are further restricted to white men, aged 40-59, because the

NHANES data contain insufficient observations on non-whites to

evaluate the form of the relationship among non-whites.  This

severely limits this analysis because both blood pressure and

blood lead levels are higher among non-whites than whites.**

     The fact that other sources of  lead, especially gasoline,

would slowly decline even without new EPA drinking water standards

created a slight complication.  Because gasoline lead levels

fall over time  as unleaded gasoline  replaces leaded, the difference

in blood lead levels resulting from  this rule will change over

time.  The estimates in this report  account for both the reduction
*   The specific coefficients and the basis  for  their derivation
    are described  in  the Addendum to the Criteria Document,  1986,
    which  is  included in Volume  1 of that publication.  The  issue
    of site adjustment is  summarized briefly on  p.  IV-lOff of  this
    document.

**  In other  EPA analyses,  e.g., Methodology for Valuing Health
    Risks  of  Ambient  Lead  Exposure  (US-EPA,  1986a),  less-conserva-
    tive assumptions  have  been made —  i.e., assuming that the same
    cardiovascular risks apply to black men  as to white men  of the
    same age  (cf.,  pages 5-5  ff).   Extending this current analysis
    to black  men,  even using  the same coefficients  and assumptions
    as for white men, would raise the estimated  benefits.

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                               IV-3 5

 in blood pressure over the past decade and reductions in some
 other sources of lead.  This model served EPA also in its analy-
 tical efforts supporting the most recent phasedown in the amount
 of lead  permitted in leaded gasoline;  it is discussed more fully
 in The Costs  and Benefits of Reducing  Lead in Gasoline (US-EPA,
 1985b).   The  coefficients were  adjusted for site-variation as
 discussed in  the Addendum to the Criteria Document (US-EPA,  1986;
 p.  A-13ff).

 IV.A.4.a.  Hypertension
      Based upon  the  studies relating lead exposure to blood
 pressure, discussed  above,  estimating  the change  in the  number of
 cases  of  hypertension  was  straightforward:   the logistic regres-
 sion  coefficients  from Pirkle et al. (1985)  adjusted for site were
 applied to the NHANES  II  data to predict  the  changes in  the  numbers
 hypertensives as a result  of reducing  the Maximum  Contaminant
 Level  (MCL) for  lead in drinking water.   In  this analysis, EPA
 estimates that there would  be 130,000  fewer  cases  of hypertension
 among males aged 40-59 in  sample  year  1988 as a result of  this
 rule.  The change due  to this proposed  regulation  was  calculated
 by subtracting the number at the  new lead  level from the number
 at the original lead level.  This estimate covers  only males  aged
 40 to 59, but includes non-whites as well as whitest

 IV.A.4.b.  Myocardial Infarctions, Strokes, and Deaths
     Estimating the impact of reduced blood pressure on morbidity
and mortality required several additional steps.   Using the NHANES

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                              IV-3 6

II data and the site-adjusted regression coefficients described
earlier, we simulated the changes in individual blood-pressure
levels due to reductions in lead from drinking water.  Coefficients
from two large studies of cardiovascular disease were then used to
estimate changes in the numbers of first-time myocardial infarc-
tions, first-time strokes, and deaths from all causes.
     The relationships between blood pressure and -cardiovascular
diseases have been established by several large, long-term epidemic-
logical studies.  The classic study, which was important in
establishing cholesterol as a major factor in the risk of heart
disease, was the Framingham study  (McGee et al., 1976).  Extensive
analyses of these data have yielded estimates of cardiovascular
risks  associated with several variables, including  blood pressure.
Figure IV-1 shows the age-adjus.ted rates of death and heart  attacks
as  functions of blood pressure  from that study.
      In the 1970s, the National  Institutes of Health funded  the
Pooling Project  (The Pooling Project Research Group, 1978),  which
combined the Framingham  data with data  from  five  other  long-term
studies to improve the  accuracy of the  risk  coefficients  for heart
attacks.   The  Pooling Project  tested the Framingham coefficients
against the other  study  results and  found  that  their predictive
power was  good.  It  then analyzed the  first  occurrence  of  myoear-
dial infarctions  in  white men  who entered  the studies at  ages 40
to 59 and  who were followed for at least  10  years.   The estimates
of the numbers of  first-time myocardial infarctions in this study
employ the Pooling Project's coefficients.

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                                    IV-3 7
                                 FIGURE IV-1


Adjusted Rates of  Death and Heart Attacks  versus Blood Pressure:
                              Framingham  Data
                 ANNUAL INOXENCE OF DEAIH BY DIASTOLIC BDOGD PRESSURE
       a
       (4
       o
       04

       o
       o
       o
       14
250



225



200



175



150



125



100
Males 45-74 (age adjusted rate)






^
»

















                <70   70-  75-  80-  85-  90-  95-  100- 105-  110+

                      74   79   84   89   94   99   104  109



                 ANNUAL INCIDENCE CP MBXftRDIAL INFARCTION BY DIASTOLIC BLOCD PRESSURE


                   Males 45-74 (age adjusted rate)
       o
       o.

       o
       o
       o
       §
      •o
      •H
       O

      5
  100 -



   90



   80



   70 -




   60



   50



   40
                  <70  70-  75-  80-  85-  90-  95-  100- 105- 110+

                       74   79   84   89   94   99   104  109

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                              IV-3 8

     In addition to estimating the risk of heart attacks, the
Framingham study estimated regression equations for the risks of
stroke and death as functions of blood pressure and other vari-
ables.  Because the Pooling Project did not include those end-
points, the Framingham study coefficients are used in this
analysis.  As with heart attacks, the estimates for strokes cover
only first-time events; thus, the estimates for strokes and
myocardial infarctions are biased downwards because they exclude
second and subsequent heart attacks and strokes associated with
elevated blood pressure.  The regression equation for deaths
covers all CVD-related causes of death; it includes deaths not
just from myocardial infarctions and strokes, but also from other
causes associated with blood pressure  (e.g., heart diseases other
than myocardial infarctions).
     Levy et al. (1984) recently tested the Framingham study
regression coefficients to see how well they explained the observed
decrease in cardiovascular mortality in the United States from
1970 to 1980.  They found that the coefficients, when coupled
with changes in blood pressure and other cardiovascular risk
factors over that same period, were able to explain about 80
percent of the drop in cardiovascular mortality.
     There is also clinical evidence showing that increased (or
decreased) blood pressure can be associated with cardiovascular
events and mortality rates.  For instance, the Hypertension
Detection and Follow-up Program  (New England Journal of Medicine,
1982) found that intervention resulting in about a 5 mm Hg change
in diastolic blood pressure produced a 20 percent reduction in

-------
                               IV-39

 overall mortality.   The Australian National  Trial  on mild hyper-
 tension also  found  reductions  in morbidity and mortality resulted
 from  lowered  blood  pressure  (Lancet,  1980).   The Multiple Risk
 Factor Intervention Trial  found that  drug therapy  to lower blood
 pressure  reduced  cardiovascular disease  in persons with normal
 resting electrocardiograms  (ECGs), but increased it in  persons
 with  abnormal resting ECGs  (Journal of the American Medical
 Association,  1982).  This  suggests an adverse effect of the drugs
 used.
      To produce estimates  for  all 40  to  59 year old white males,
 the individual risk of each person sampled in the  NHANES II was
 summed and then averaged.  Since the  sampled  individuals repre-
 sent  the U.S. population for their specific  age-race-sex category,
 their average risk  represents  the average risk for all  40 to 59
 year-old white men.  Because blood lead  levels have dropped since
 the NHANES II period, we corrected for that change and  then evalua-
 ted the effects of  the potential MCL  for lead.  Again,  only
white men were examined because there were too few blacks  in the
Framingham study, and their risk might be different from whites.
     The three cardiovascular-risk regression equations  all  predict
risk over the next  10 years, given current blood pressure,  age,  and
other characteristics.   Presumably, the risk  in years 2-10  was
affected by blood pressure in  those years as well  as by  initial
blood pressure.   Because blood pressure levels over  time  in  the
same individual are positively correlated, it is likely  that
the regression coefficient in part included the effect of future
blood pressure levels.   Lacking any data with which  to estimate

-------
                               IV-40

the pure effect of a one-year change in blood pressure, we divided
the coefficient for 10-year risk by 10.  The adjusted coefficient
was then used with the year-by-year predicted changes in blood
pressure to estimate risk reductions.  This procedure almost
certainly overcompensates, lending a downward bias to the results,
because current blood pressure is not perfectly correlated with
future blood pressure.
     In this analysis, we adjusted the population at risk for the
increases in the U.S. population of white males aged 40 to 59.
The regression from the Framingham study predicting deaths for
men aged 40 to 54 was extended to 40 to 59 for data comparability
and uniformity.  Because the death rate actually increases with
age, this also will bias the results downward.
     In this analysis, EPA estimates that there would be 240  fewer
rayocardial infarctions, 80 fewer strokes, and 240 fewer deaths
among the members of the target groups in sample year 1988 as a
result of the potential MCL.  Extending this analysis to men  of
other ages and to non-whites would substantially increase these
estimates.
IV.B.  Lead's Effects upon Reproductive Function
     At high levels,  lead's  adverse  effects upon human reproductive
function have been known  for over  100  years.*  In 1860, for
instance, Paul published  findings  that lead-poisoned women were
likely to abort or deliver stillborn infants, and articles in the
1880s reported lead  to be a  teratogen.  Because  lead passes  the
 *   Indeed,  'lead  plasters'  were used as abortifaeients at the turn
    of  the century.

-------
                               IV-41

 placental barrier,  the most sensitive population for lead exposure
 may be fetuses and  newborn infants, whose source of exposure to
 lead is,  of course, the mother.   Lead has been implicated in com-
 plications of  pregnancy,  including early and stillbirths, and
 possibly  low-level  congenital anomalies.   The effects upon the
 fetus  and neonate are  discussed  in Section III.C.,  above.  In
 this section,  we summarize some  of the reproductive effects upon
 women  and men,  but  estimates  of  populations at risk are  made
 only for  women.  The Criteria Document (1986;  p.  12-192  ff)
 contains  a full discussion of lead's  adverse effects upon
 reproductive function.   In addition,  the  Addendum to the Criteria
 Document  (1986; p.  A-31  ff) contains  a section on growth and
 developmental  effects  following  pre-natal lead exposure,  including
 some studies of negative pregnancy outcomes.
     Because several early studies (many  from  the 1800s)  showed
 clear  adverse effects of lead  at high  levels upon female  reproduc-
 tive functions, particularly  miscarriages and  stillbirths, women
 have been  largely — though not entirely  —  excluded  from occupa-
 tional exposure to  lead.   The mechanisms  underlying  these effects
 are unknown at this time.  Factors which  could  contribute range
 from indirect effects of lead upon maternal  nutrition or  hormonal
 state before or during pregnancy to more  direct gametotoxic,
 embryotoxic, fetotoxic, or teratogenic effects  that could affect
parental fertility or off-spring viability during gestation.
     In addition,  pregnancy is a stress that may place women at
higher risk for lead toxicity, because both iron deficiency
and calcium deficiency increase susceptibility to lead, and

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                               IV-4 2

women have an increased risk of both deficiencies during pregnancy
and post-parturition (Rom, 1976).  Pregnancy and lactation are
also physiological conditions of bone demineralization, when
lead as well as calcium and other minerals are released from
storage in bones.  While this may decrease the total body burden
of lead for the pregnant woman, it obviously has potentially
toxic consequences for the fetus.
     However, there is inadequate information to assess precisely
the effects of lead exposure — at either high or low  levels of
exposure — on human ovarian function or other factors affecting
female fertility, or on maternal variables, such as hormonal
levels, that are known to affect the ability of the pregnant
woman to carry the fetus  successfully to full term.
     While earlier studies focused more upon women, much
research is now  directed  to  lead's  effect upon male reproductive
function.*  Lead-related  interference with male reproduction
function,  including gonadal  impairment, diminished  number and
viability  of spermatocytes,  and  apparently exposure-related
 increases  in erectile  dysfunction,  have been  reported. Also,
 there  are  several  articles  implicating  exposure of  males  to  lead
 as the cause of  adverse  effects  on the  conceptus  (e.g., Singhal
 and Thomas,  1980).  These include  low fertility  rates, low birth
 weights,  and higher rates for miscarriages  and  stillbirths in
 families  of  occupationally lead-exposed men.
 *  As an indication, the chapter on reproductive effects in Singhal
    and Thomas (1980) discusses males almost exclusively.

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                              IV-4 3


IV.B.I.  Estimating the Population At-Risk
         for Female Reproductive Effects

     While lead is a fetotoxin and therefore probably dangerous

to the unborn even at low levels of exposure, the only data on

reproductive effects upon the adult female (as opposed to the

fetus)* are at fairly high levels, i.e. > 15 ug/dl.  No studies

have been conducted on reproductive effects of women with 'normal'

lead exposures.  Recent studies (discussed in the previous chapter)

on the inverse relationship between blood lead levels and gesta-

tional age and birth weight and height suggest that reproductive

effects of lead exposure observed at high blood-levels continue

through the 'normal' range.  The available data concerning lead's

adverse health effects indicate that the lack of data on reproduc-

tive effects at low exposure levels reflects a lack of data and

not a finding of no effect.
                       *
     To assess the adult female population potentially at risk of

suffering reproductive effects, we calculated the number of women

of child-bearing age (i.e., aged 15-44) above 15 ug/dl who would

benefit from this proposed rule.  While there is evidence of neuro-

logical effects, enzymatic inhibition and metabolic alterations at

below 10 ug/dl,** this cut-off was used because at 15 ug/dl, many

body systems (e.g., heme synthesis) show indications of significant

impairment.  This estimate should be understood, therefore, as a
*   Fetal effects related to lead exposure are discussed in
    Chapter III.

**  The Addendum to the Criteria Document (1986) says, "At present,
    perinatal blood lead levels at least as low as 10 to 15 ug/dl
    clearly warrant concern for deleterious effects on early post-
    natal as well as prenatal development." (p. A-48)

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                              IV-4 4


low estimate of potential adverse effect.  All women of childbearing

age and with blood lead levels over 15 ug/dl were considered to be

at risk of reproductive effects whether or not they were pregnant,

because the damage occurs in any ease.

     In Section C of Chapter III, estimates are presented of the

number of women of childbearing age, i.e., aged 15 to 44 (24 per-

cent of the total population), and the fraction of them estimated

to have blood lead levels over 15 ug/dl in 1988 (0.36 percent).

Of the total current U.S. population of a little over 240 million,

219 million people are served by community water supplies, of

whom 42 million receive water that exceeds a potential MCL of  20

ug/1.  Assuming that women of childbearing age and that women  with

high blood-lead levels are distributed proportionately throughput

the population,*


               219
          24% x 240 million x 0.36% x  42 million = 33,000


women  in  1988 will be _>  15 ug/dl  and,  therefore, at  risk from

suffering reproductive effects  from exposure  to  lead.  By  reducing
 *  While  it  is  reasonable  to assume that women of child-bearing age
   are  distributed proportionately throughout the population and
   therefore that they are equally at-risk of receiving water with
   high lead levels,  it is very conservative to assume that women
   with high levels of lead in their blood are equally distributed
   in areas  with high water-lead levels and low water-lead levels.
   This is because blood lead levels are one measure of lead
   exposure; in general, women with high blood-lead levels are
   exposed to more lead.  Because drinking water is one source of
   exposure, it is more likely that — all other sources being
   equal —  women receiving more lead in their drinking water_
   will have higher than average blood-lead levels.  While this
    is logical,  there is no empirical data to calculate the increased
    likelihood.   We have used the most conservative assumption:
   proportional distribution.

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                            .   IV-45


 the contribution of lead from drinking water,  this proposed rule

 will provide  benefits to these women in the form of reduced risk

 of  potential  reproductive effects.

      Also,  as presented  in Chapter  III, to assess the  number of

 pregnant  women at risk of suffering adverse effects as a result

 of  exposure to lead from drinking water that exceeds the proposed

 MCL,  we assumed that pregnant women were distributed proportion-

 ately throughout the country  and therefore used  the national

 occurrence  data to estimate this at-risk population.   Of the

 estimated 54  million women of childbearing age  (15-44),  about

 7 percent are likely to  be pregnant at any given time.*   Of these,

 680,000 are now probably receiving  water that exceeds  the proposed

 MCL.



 IV.C.  Monetized Estimates  of Adult Health Benefits;
       Reduced  Cardiovascular Disease  Risk in Men

     Valuing  reductions  in  morbidity and mortality  is  a  diffi-

 cult  and, to  say the  least, controversial  task.  For morbidity,

 the benefit estimates  included avoided medical costs and  foregone

 earnings associated with  the  diseases.   This underestimates  social

 benefits because  they  fail  to  account  for  other  important losses

 associated with  disease,   including  long-term effects,  pain  and

 suffering (including,  for  instance,  the  paralysis that often

 follows a stroke).  For valuing the  reduction in mortality  risk,

we have chosen a  fairly conservative estimate ($1 million per life)
*  The rate, according to the Census Bureau, is currently 67.4
   pregnancies per 1,000 women of child-bearing age.

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                               IV-46

from the large range obtained from studies of occupational risk
premiums and from other EPA policy papers.

IV.C.1.  Hypertension
     Whether or not it results in coronary or cerebrovascular
disease, high blood pressure is a significant chronic illness.
It also generates economic costs, in the  form of drugs, physi-
cians' visits, hospitalization, and work  loss.  Data from the
NHANES II and from the National Institutes of Health were used to
estimate the value of avoiding a case of  high blood pressure.
     The NHANES II ascertained how many times per year a person
saw a physician because of high blood pressure.  The weighted
average, for males 40 to  59 years old with diastolic blood pres-
sure over 90 mm, was 3.27 visits per year.   Based upon an average
cost of $35 per physician visit, the annual  total is $114.
     The same population  was  forced to  remain  in bed an  average
of 0.41 days per year because of high blood  pressure.  At the
average daily wage  ($80),*  that  translates  to  $33 per year.
Data  from the NHANES II  also  show  that  29 percent of those
clinically  defined  as  hypertensive were on  medication  for hyper-
tension.  Using  standard medical costs  indicating that  the  average
drug cost  is  $220 per  year for  those  on medication  yields an
annual cost of  $64  (in 1985 dollars).
 *  Based upon wage and earnings data in Statistical Abstracts of
    the U.S. 1985 and the Economic Report of the President 1986.

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                               IV-47

      The National Hospital Discharge Survey (1979) found that,
 excluding those with heart disease or cerebrovascular disease,
 people with high blood pressure used 3.5 million of the occupied
 hospital bed-days that year;  dividing by the 60 million people"
 the NHANES II identified as having high blood pressure gives a
 rate of 0.058 hospital bed-days per person per year.   We have
 assumed that these results apply to the 40 to 59 year old age
 group of males,  as well.   Using a daily hospital cost of $450,
 the annual cost  per hypertensive is $26.
      Summing these estimates  yields a total of $237 per hyper-
 tensive per year (1985 dollars).   It should be noted  that only 29
 percent of the people  with blood pressure above 90 mm in the
 NHANES II  were on blood pressure medication,  in part  because some
 of  them had not  previously been detected  as having high blood
 pressure.   Therefore,  the  average cost for a  detected case  will
 be  higher.   For  example, Weinstein and Stason  (1977)  used an
 average cost of  $200 in 1975  dollars,  or  about $486 in 1985
 dollars, for treatment of  patients undergoing  medical  care  for
 hypertension.  Nevertheless,  we  have  conservatively used  $250  as
 the value  of  avoiding  one  case of  high blood pressure  for one
 year.

 IV.C.2.  Myocardial Infarctions
    The estimate of the benefits of reducing the incidence of
myocardial  infarctions  relies heavily  on Hartunian et  al. (1981),
who estimated the medical expenses and lost wages associated with
a variety of diseases.   Under the  category of myocardial  infarc-
tions  (MI), Hartunian et al. examined three types of cases:

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                              IV-4 8


sudden death, fatal MI, and nonfatal MI.  ("Sudden death" was

classified as a myocardial infarction in the Pooling Project

regression coefficients.)

     For each category and each age group, Hartunian et al.

obtained data on the type of medical services needed (e.g., ambu-

lance or coronary intensive care unit), the fraction of cases

using each service, and the costs  in 1975 dollars.  They also

determined the annualized recurrence and follow-up costs, by age,

for each condition.  These were then discounted  (using a 6 percent

real discount rate) to the time of  initial occurrence to estimate

the cost, in current dollars, of  each new case.  The resulting

estimates were $96  for sudden death and $7,075 for both  fatal and

nonfatal Mis.

     These 1975  estimates have been adjusted  in  three ways  to

reflect current  conditions.  First, they  are  inflated to 1985

dollars.  Because most of the costs were  hospital-related,  with

the rest principally  being physicians'  fees,  we  inflated the

Hartunian et al. cost  estimates  by a weighted average of 80

percent of  the  change  in the Consumer  Price Index (CPI)  for

hospital  rooms  and 20  percent of the  change in the  CPI  for

physicians'  charges.*  Approximately  90 percent of  the  Hartunian

et al. MI  costs were  hospital-related,  not physicians'  fees,  and

hospital  costs rose faster than physicians' fees, lending  a down-

ward  bias to the estimates.
 *  Using data from Tables B-56 and following, Economic Report of
    the President 1986.

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                               IV-49





      The second adjustment in the 1975 estimates involves changing



 cost indices.  Because cost indices only account for increased



 costs of the same procedure, in this case principally the initial



 hospitalization for a heart attack, they do not reflect the cost



 of new or different procedures.   Since 1975, the fraction of people



 suffering coronary heart disease who subsequently undergo coronary



 bypass operations has increased  substantially.  The number of by-



 pass operations tripled in seven years, from 57,000 in 1975 to



 170,000 in 1982,  while the number of cases  of coronary heart



 disease has remained relatively  constant (National  Centers for



 Health Statistics,  Hospital Discharge  Survey,  and unpublished



 data).   Based on  the Hartunian et al.  data,  7.1 percent of MI



 cases  in 1975 had  subsequent bypass  operations.  Assuming  that



 they shared proportionately in the tripling  of the  bypass  opera-



 tion rate,  we estimated  that an  additional 14  percent  of Mis now



 result  in a bypass  operation.  Hartunian  et  al.  estimated  the



 cost of  bypass  operations  at $6,700  in  1975  dollars, or  $18,200



 in 1985  dollars.  Adding 14 percent  of  this  cost to the  other



 direct costs  yields  an estimate  of the  total direct costs  in



 1985 dollars  of $21,700 for an MI  and $260 for  sudden death.



     The  third adjustment  involved discount rates.  Hartunian



 et al. used a 6 percent real discount rate to present value  the



 future year costs, whereas this analysis employs a 10 percent



discount rate.  Fortunately, Hartunian et al. performed sensi-



tivity calculations for other discount rates, including 10 per-



cent.  Making all of these adjustments, the costs per case are



$19,600 for an MI  and $233 for sudden death.

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                              IV-50

     Hartunian et al. also obtained data indicating the proba-
bility distribution of cases among the different categories.  Of
the total number of cases in these three categories, about 22.5
percent were sudden deaths and the remaining 77.5 percent were
fatal or nonfatal Mis.  Applying those percentages to the
medical-cost estimates derived above yields a weighted average
of $15r230 per myocardial infarction.
     Hartunian et al. calculated the present value of fore-
gone earnings based  on reduced labor force participation using
data on each type of heart disease, broken down  by sex and  10-year
age categories.  Those results are used  here, with several  modi-
fications.  First,  foregone  earnings for fatal heart  attacks  are
excluded because the reduction  in  mortality  risks  is  valued
separately  (see  Section  IV.C.4., below).  Second, we  adjusted
for  the  increase in average  non-farm compensation  from 1975 to
1985, using information  from Data  Resources,  Incorporated;  from
the  U.S.  Census  Bureau;  and from the Economic Report  of  the
President to Congress.   Finally, again a discount  rate of 10 per-
 cent was used,  rather than the 6 percent used by Hartunian et al.
      The resulting estimates of foregone earnings  are $97,000 for
 heart attack victims under 45; $51,000  for those between 45 and
 54;  and $24,000 for those over 55.  Based on data from the
 Pooling Project and NHANES II, 16.1 percent of  nonfatal heart
 attacks in men between 40 and 59  occur  in those under 45, 50.9
 percent occur in those between 45 and 54, and 33 percent in  those
 55 and older.  Using those percentages  yields a weighted average
 for lost earnings of $49,500 per  attack.  Combining  that earnings

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                               IV-51

 estimate with the earlier one for medical costs yields a total
 benefit per myocardial infarction avoided of about $65,000 (in
 1985 dollars).

 IV.C.3.   Strokes
      The estimates of  the benefits of  avoiding strokes also rely
 on Hartunian et  al., with similar adjustments.  (Unlike myocardial
 infarctions,  the medical  cost estimates  for strokes  were not
 adjusted to reflect any changes  in medical treatment since 1975.)
 Table  IV-1  presents the estimates for  three types  of stroke ~
 hemorrhagic,  infarctive,  and  transient ischemic attacks (TIA)  —
 by age.   The  averages  are based  on the distribution  of types of
 strokes  and incidence  of  strokes by age.   The  overall average  is
 $48,000  per stroke  avoided, in 1985  dollars.
     We  have  been unable  to estimate a value for avoiding the
 loss in  quality  of  life that  occurs  in stroke  victims.   This
 is a significant omission.  For  example,  of the people in the
 NHANES II who reported  having had  a  stroke  in  the past,  45
 percent  suffered paralysis in the  face and  13  percent still had
 at least partial  facial paralysis,  54  percent  suffered  paralysis
 in at least one  arm and 21 percent  remained paralyzed,  59 percent
 had numbness in  arms or legs and 28  percent had  remaining numbness,
 30 percent had vision impairment and 13 percent  remained visually
 impaired, and 50 percent had speech  impairment with  22  percent
continuing to suffer from speech impairment.  While  there are no
estimates of people's  willingness to pay to avoid the risk of
these profound injuries, common sense  suggests that  it  is high.

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IV-5 2
Type of Stroke
Age 	
Heitiorrhagic
35-44
44-54
55-64
Infarctive
35-44
45-54
55-64
Transient ischemia attacks
35-44
45-54
55-64
Weighted average
Medical
Expenses

$13,600
14,300
18,600

19,000
19,600
25,500

3,450
3,450
3,450

Foregone
Earnings

$44,300
28,100
11,900

76,700
46,500
15,100

1,200
3,325
8,950

Total

$57,900
42,400
30,500

95,700
66,100
40,600

4,650
6,775
12,400
$48,000

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                                IV-5 3

  IV.C.4.  Mortality
      Valuing reductions  in mortality  is highly  controversial.
  Over the past decade or  so, a  substantial  literature  has  developed
  on the subject.  Economists are in general agreement  that the
  best conceptual approach to use is the willingness-to-pay (WTP)
  of the individuals involved.  The appropriate value is not
  the amount that an individual would pay to avoid certain  death,
 but rather the total sum that a large group of  individuals would
 pay to reduce small risks that sum to one; for  example, the
 amount  that 10,000 people would pay to reduce a risk to each of
 them of one in ten thousand.
      Several  studies have estimated  WTP based on implicit tradeoffs
 between risk  and dollars  revealed  in market transactions.   Most
 of  these  studies (e.g., Thaler and Rosen,  1976;  Smith, 1974  and
 1976; Viscusi,  1978)  have studied labor markets, based on the
 premise that,  all  else being equal, workers must receive  higher
 wages to  accept  a  higher  risk  of being injured  or killed  on  the
 job.  Such  studies typically regress wages  on risk  and a variety
 of other  explanatory  variables  (e.g.,  levels of  education  required,
 worker  experience, whether or not the  industry  is unionized,
 location, and non-risk working  conditions).  In  such regressions,
 risk might  be measured as the number of fatalities  per  1,000
 workers per year.  The coefficient for that variable is then
 interpreted as the amount of extra wages needed  to  compensate
 for a 0.001 risk of death.  Dividing the coefficient by the unit
of risk  yields the estimate of WTP to avoid a statistical death.

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                              IV-5 4

For example, if the coefficient is $500, the estimated WTP is
$500,000 (- $500/0.001).
     A few studies have estimated WTP in non-occupational settings.
Blomquist (1977), for example, estimated the implicit cost-risk
tradeoffs that individuals make in deciding whether or not to
take the time to put on seat belts.
     None of these studies yields definitive answers.  All suffer
from data limitations  (e.g., incomplete  information on possible
confounding variables  and on the  extent  to which  individuals
perceive the risks they face).  Not  surprisingly,  given  these
problems, the studies  also yield  a wide  range  of  estimates.  A
recent  survey of  the  literature  prepared for  EPA  found  a range
of $400,000 to  $7 million per  statistical  life saved  (Violette
and Chestnut,  1983).   Based  on that  survey,  EPA's guidelines
 (US-EPA,  1984c)  do  not attempt to set any specific value, but
rather recommend that range.   To simplify the presentation of  the
results,  this  analysis uses  a single value from the lower end  of
 that range, $1 million per statistical life saved.  Although we
 do not present any formal sensitivity analyses on this value,  the
 results show that the net benefits are so large that they would
 remain positive whatever part of that broad range is used; even
 at $400,000 per statistical life saved, the estimated benefits
 greatly exceed the costs.
 IV.C.5.  Summary of Annual Monetized Benefits of  Reduced
          Cardiovascular Disease
      Table IV-2 summarizes the annual monetized  benefits of reduc-
 ing the numbers of cases of hypertension, myocardial infarctions,

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                                      IV-5 5
TABLE IV-2.  Sunroary of Annual Monetized Blood-Pressure

Category
Cases of hypertension

Myocardial infarctions

Strokes

Deaths

TOTAL
fmi Tin /-*vtr* 1 QOC *3^~t 1 -._— \

Sub-Population
Considered
males,
aged 40-59
white males,
aged 40-59
white males,
aged 40-59
white males,
aged 40-59

Unit
Cost
(1985
dollars)
$250

$65,000

$48,000

$1 million



Annual
Avoided
Cases
130,000

240

80

240




Total Benefits
(millions
1985 dollars )
$32.5

$15.6

$3.8

$240.0

$291.9










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                              IV-5 6


strokes, and deaths due to high blood pressure that would result

from the proposed lowering of the allowable amount of lead in

drinking water.  These are limited for several reasons:

     (1)  The hypertension estimate covers only males aged 40
          to 59.

     (2)  The other estimates cover only white males aged 40
          to 59.

     (3)  No value is assigned to reduced pain and' suffering
          associated with hypertension, myocardial infarctions,
          and strokes.

     (4)  These are the only adult health effects that are
          monetized.

     Most importantly, these estimates assume a causal link between

blood  lead  levels  and blood pressure  and assume that reducing  body

lead burden can reduce blood pressure.  In addition, of  course,

some readers may quarrel with  the  value assigned  to  reduced risk

of mortality; we have chosen a single value  for convenience, not

because any particular value can be  defended strongly.   Despite

these  limitations, the estimated annual benefits  of  this potential

rule are large,  totalling  $291.9 million  for sample  year 1988.


IV.D.   Valuing  Health Effects;   Caveats  and  Limitations

     To begin  valuing the  health effects  that would  be avoided

as  a result of  the proposed MCL  for lead  in  drinking water,  we

have estimated —  for adult males — the medical  costs,  lost

earnings, and  value  of lowered mortality risk associated with

reducing the number of hypertensives, strokes, and heart attacks

 (only  white males, aged 40-59, were included in the latter two

 categories).   We also estimated the reduction in the number of

 deaths from all causes (again, only for white males, aged 40-59)

 resulting  from'the lowered MCL.

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                               IV-5 7

      The cost-of-illness estimates themselves are low,  primarily
 because, to  reduce  potential  controversy,  the calculations
 rely on  many conservative assumptions.   For instance, Hartunian's
 estimates (used  for adult health  costs)  are based largely upon
 actual medical practice  and not preferred  treatment.  As  a
 specific example, their  panel  of  medical consultants  indicated
 that only 5  percent of stroke  victims would receive anti-coagulant
 drugs, less  than 5  percent would  receive any vocational rehabili-
 tation,  and  that most would receive little  or no  physical therapy.
 The  real  (social) cost of the  illness does  not decrease if not
 all  victims  receive  the  treatment they need;  assuming the treat-
 ments are  efficacious, stroke  victims who are  left disabled
 incur a  cost at least equal to the  cost of  the .medication they
 should have  (but did not) receive.  The health benefit estimates,
 therefore, should be understood as  very low  lower-bounds  for
 these categories of effects.
     Cost-of-illness calculations were not conducted for most  of
 the adverse health effects associated with human exposure  to
 lead including the reproductive effects in both males and  females
discussed qualitatively in Section C.  Among the many other
effects not valued monetarily  in this health benefit analysis are:
     - kidney effects, detectable in children at blood lead
       concentrations of  about 10  ug/dl,  although the  damage is
       often not manifest until adulthood;
     - hematopoietic damage,  detectable in  children at levels
       below 10  ug/dl;
     - adverse pregnancy  and  other reproductive effects  in women,
       no threshold  indicated;

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                             IV-58

    - nervous system effects in adults, with behavioral functions
      disturbed  at very high levels,  a dose-dependent  slowing
      of nerve conduction velocity  in occupationally-exposed
      workers, and peripheral  nerve dysfunction  at  30-50 ug/dl
      (central nervous system  effects are  detectable  in children
      at 10 ug/dl);
    - metabolic  changes, detectable in children  at  about 12 ug/dl;
    - enzymatic  inhibition, with  no threshold  indicated  in adults
      or children, even below  10  ug/dl;
    - all  effects on  fetuses,  although  lead crosses the placental
      barrier  and maternal  blood-lead values correlate with
      several  adverse outcomes,  including  fetotoxicity at
      high levels and brain damage  at lower levels;
    - cardiovascular  effects  on older men  and  black males  of
      all  ages,  which may  be  dose-dependent with no threshold;
    - genetoxic  and  carcinogenic effects of lead;
    -  lead's effects  upon  the immune  system; and
    -  lead's effects  upon  other organ systems  (e.g., gastro-
       intestinal) .
     Finally, three serious phenomena of lead's adverse effect
upon human health were ignored.  First,  hematopoietic, metabolic,
and enzymatic damage have cascading effects throughout the body,
which have not been adequately addressed.  Second, many of the
specific effects have long-lasting sequelae which are not  included,
And last, there  is a significantly greater chance of serious
effects later in life, including renal failure and  cerebral
palsy, even in individuals whose highest detected blood-lead

-------
                               IV-5 9

 level was below that associated with the most severe effects
 and who did not at the time show evidence of lead toxicity;
 this increased risk also was not included.
      In addition to all the categories of adverse health effects
 for which we have not yet been able to quantify benefits at all,
 the costs of the illnesses that were calculated greatly under-
 estimate the real (social) benefits of preventing those effects,
 even for the health categories evaluated.  The underestimates
 occur because some categories of direct costs associated with
 those effects were excluded,  as were all indirect but related
 costs.
      In general,  society's willingness-to-pay to avoid a given
 adverse effect is many times  greater than the cost of the illness
 itself,  so  cost-of-illness analyses  inherently underestimate
 the  benefits  of  avoiding  the  adverse effect.*  Willingness-to-pay
 studies  indicate  that  society is  usually willing to pay two to
 ten  times the cost of  medical treatment,  and  that in specific
 circumstances society  is  willing  to  pay  a hundred or a  thousand
 times  the cost of  the  illness itself in  order to prevent its
 occurrence.
     More specifically, in  the cost-of-illness  analyses,  only
 expenses that  are  directly  related to an  individual's medical
 treatment for  the  specific  symptom being  evaluated,  at  the  time
 the symptom occurs, were  included.   So,  for instance, no  costs
were ascribed  for  the possibility of adverse  effects from the
*  For instance, in general people would be willing to pay more
   than the price of two aspirins to avoid having a headache.

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                              IV-60


medical treatment itself or for the possibility that the specific

effect of lead may precipitate or aggravate other health effects

(e.g., heart attack and stroke victims are at increased risk of

respiratory illness).  Related expenses, such as the costs incurred

by partially paralyzed stroke victims in purchasing specially

designed appliances or retrofitting their existing possessions,

or the costs of adapting the home environments  for victims of

CVD were also excluded.  Finally, no value was  ascribed to the

pain  and suffering of those affected; this is an especially

significant omission because, as an example, about half of stroke

victims are permanently  incapacitated or paralyzed.

      All the indirect but  related costs of lead's adverse effect

upon  human health were also  left out.  These  include  work time

lost  by friends and  relatives o.f the victims  (including spouses);

medical research  related to  the prevention,  detection,  or  treatment

of  the effects  of exposure to  lead;  the development  of  new  pro-

cedures  to  correct  the damage  resulting  from lead  exposure;  •

decreased  future  earnings for  those suffering  cognitive damage  or

physical  incapacitation  (including behavioral  disorders)  from

 lead's  adverse  effects upon virtually every human  system;  and the

 like.


 IV.E.  Summary of Annual Monetized and Non-Monetized Adult Health
        Benefits of Reducing Exposure to Lead in Drinking Water

      This chapter discussed two major physiological effects

 resulting from exposure to lead:  cardiovascular changes in males

 aged 40 to 59 and reproductive impairment in women of childbearing

 age.  Of these, only the male cardiovascular effects were monetized,

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                              IV-61





Estimates of the number of women at-risk of reproductive effects,



as well as the number of fetuses potentially at-risk, were presented



but no monetary value was ascribed to them.  Table IV-3 summarizes



the annual monetized and non-monetized benefits of a potential



reduction in the MCL for lead for one sample year, 1988.

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                                      IV-6 2
TABLE IV-3.  Summary of Annual Monetized and Non-nonetized


Effect 	


Sub-Population
Considered
Unit
Cost Annual
( 1985 Cases
dollars) Avoided
-
Benefits
(millions 1985
dollars)
MONETIZED MALE BLOOD-PRESSURE RELATED EFFECTS
Cases of hypertension

Myocardial infarctions
Strokes

Deaths

TOTAL
males,
aged 40-59
white males,
aged 40-59
white males,
aged 40-59
white males,
aged 40-59

$250 130,000

$65,000 240
$48,000 80

$1 million 240


$32.5

$15.6
$3.8

$240.0

$291.9
NON-MONETIZED FEMALE REPRODUCTIVE EFFECTS
Adverse reproductive
effects

women,
aged 15-44
>15 ug/dl
NA 33,000

NA

(Pregnancies at risk)
(of adverse effects )
( - same as at-risk )
(    fetuses        )
pregnant women,
aged 15-44
                                              NA
680,000
                                                                    NA)

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                          CHAPTER V

            BENEFITS FROM REDUCED MATERIALS DAMAGE


     This chapter contains a discussion of the materials benefits

that will result from reducing the occurrence of lead in drinking

water.  Lead seldom occurs naturally in source waters;* primarily

it is leached from the pipes and solder by corrosive water.**

Therefore, reducing the occurrence of lead in public water supplies

means reducing the corrosivity of that water.+  Reducing the

corrosivity of the water produces materials benefits in the form

of decreased corrosion damage, in addition to the decrease in

lead.  This chapter discusses the characteristics of corrosive

water and contains estimates of the potential savings that could

accrue to water utilities and to consumers by lessening the

corrosivity of their water.

     As discussed in Chapter II, the major source of lead contami-

nation of drinking water are the materials of the water distribution
*  Concentrations of lead in ground water in the United States
   are typically low.  Lead naturally occurring in surface waters
   or contributed to water by auto emissions, surface run-off,
   etc. will generally settle in the sediments before reaching
   the consumer.

** Corrosion is the deterioration of a substance or its proper-
   ties due to a reaction with its environment.  In this document,
   the "substance" that deteriorates is the pipe — whether made
   of metal, asbestos-cement, cement, or plastic — and the flux
   and solder joining the pipes, and the "environment" is water,
   i.e., we are concerned with internal corrosion.  (Pipes and
   other water treatment equipment can also corrode externally.)

+  An alternative, of course, is to replace all plumbing materials
   containing lead.  This would be extremely expensive, costing
   probably several hundred billion dollars.  (Based upon an
   estimated average replacement cost of $3,000-$5,000 each for
   most of the 85 million housing units in the country, and
   $1,500 for each of the 1-10 million housing units estimated to
   be likely to have a lead service connection.)

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                                V-2


and home plumbing systems.  Lead occurs primarily as a corrosion

by-product.  An analysis of the benefits of reducing lead in public

water supplies must, therefore, include the benefits of reducing

the source of the contamination, that is, the corrosivity (or

aggressiveness) of the water.

     While pipes made with lead are often considered the source of

lead in drinking water, many studies show that lead solder joints

actually contribute considerable amounts, as well.  In fact, the

data show that newly-installed lead soldered pipes conveying

corrosive water may leach much more lead than older lead pipes.

In addition, lead may also leach from brass faucets.  These

issues are also discussed in Chapter II.

     The corrosivity of drinking water is important for two main

reasons:  aggressive water may create or have adverse health effects

and the water may cause the plumbing system to deteriorate.  Cor-

rosion also affects the aesthetic quality of the water, by stain-

ing fixtures, 'discoloring water (most commonly 'red water1), and

causing a bad taste.

     Corrosive water can be a health problem* because it leaches

contaminants from the supply pipes and distribution system'  and

increases the concentrations of metal compounds in the water.

In addition to lead, the metals cadmium, zinc, copper and iron

are used in plumbing materials and occur in drinking water as

corrosion by-products.
*  The potential relationship between corrosive water and cardio-
   vascular disease  is discussed  in Chapter  IV.

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                                V-3


     Section V.A. contains a discussion of what makes water

corrosive: the characteristics of aggressive water, the chemistry

of corrosivity, and corrosion indices.  In Section V.B. , several

analyses of the extent of damage to public drinking water systems

from internal corrosion are described, and at the end of the

section, these analyses are used to quantify the benefits of

reducing the corrosivity of U.S. public drinking supplies.

     The Safe Drinking Water Act requires EPA to set limits, Maxi-

mum Contaminant Levels (MCLs), for drinking water.  The National

Primary Drinking Water Regulations require that these limits

be met at the free-flowing outlet of the ultimate user.  Because

many metals (including lead) occur in drinking water primarily

as corrosion by-products, the degree of corrosivity of a system's

water is an important consideration in meeting the MCLs at the

tap.  However, it is difficult to predict a water's potential

corrosivity.  In addition, much of the problem of corrosion is

associated with home plumbing.*  EPA has not established guidelines
* Utilities are responsible for the integrity of the distribution
  system and the .quality of the water delivered to customers.
  But there are many factors adversely influencing end-use water
  over which they have no direct control.  These include the age
  and condition of the mains and service connections (many older
  cities have lead pipes), the fact that consumers want soft water
  (because it is easier to make suds), local building codes often
  required the use of lead solder to join copper pipes in construc-
  tion (the combination of copper and lead results in galvanic
  corrosion), the condition of residential plumbing, the age and
  condition of the solder throughout the system (lead is leached
  quickly from newly-applied solder), and generally poor monitoring
  of end-use water.  Finally, most utilities have little control
  over the financial resources available to correct identified
  problems:  both their spending and rate structures are usually
  regulated either by the local government or by a public utility
  commission.

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                                V-4





for corrosivity.  However, EPA did require utilities to monitor and



test for corrosivity characteristics using the Langelier Saturation



Index (see Section V.A.4. below), and to identify and report on



all materials used within the distribution system by February



1983.  The purpose of this one-time event was to identify circum-



stances where corrosion contamination was likely to occur, and



to encourage appropriate corrective action.



     The 1986 Amendments to the Safe Drinking Water Act included



a provision banning the use of materials containing lead in public



water systems and in residences connected to public water systems.



While the ban is effective immediately, States have up to two years



to enforce the ban.





V.A.  The Characteristics of Aggressive Water



     Corrosivity is a complex characteristic of water primarily



related to pH, alkalinity, dissolved oxygen, total dissolved



solids, hardness, velocity, temperature, and other factors.



All water is corrosive to some degree.  How aggressive a water



is depends on its physical and chemical characteristics as well



as what substance(s) it comes in contact with — water that is



extremely corrosive to some materials may be less corrosive to



others.  Usually, corrosion is considered a potential problem



only for metals, but non-metallic substances (such as asbestos/



cement or cement-lined pipes) can also deteriorate when in contact



with water.



     Corrosion occurs because of physical and chemical actions



between the plumbing materials and the water.  The actual

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                                V-5


mechanisms of corrosion are usually a complex and interrelated

combination of physical, chemical and even biological factors.


V.A.I.  Parameters of Water Affecting Corrosivity

     The following discussion of the characteristics of water

that affect corrosivity summarizes the more detailed presentations

in Internal Corrosion of Water Distribution Systems (AWWA-DVGW,

1985), the Corrosion Manual for Internal Corrosion of Water

Distribution Systems (EPA, 1984; p. 11-16), and Larson (1975).


     PHYSICAL CHARACTERISTICS; The two main physical characteris-

tics that affect corrosion are flow velocity (which can either

increase or decrease the corrosion rate depending on other

properties of the water) and temperature (generally, the higher

the temperature, the greater the corrosion rate).


     CHEMICAL CHARACTERISTICS;  Most of what is called corrosion

is caused by chemical or electrochemical actions.  Many of the

chemical factors affecting corrosion rates are related, and a

change in one may change others.

     pH* is a measure of the concentration of hydrogen ion, H+,

in the water, which is important because- H+ is one of the major

substances that accepts the electrons given up by a metal when

it corrodes.   In general, at lower pH levels « 6.8), most metals

will corrode more rapidly than at higher pH levels (> 9.0).  How-

ever, under certain conditions corrosion can occur at high pH.
*  This definition is based upon the discussions in Schock and
   Gardels, 1983 and US-EPA, 1984.

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                                V-6

Corrosion can also occur throughout the range of 5-9 if no protec-
tive film is present.  pH may not have a strictly linear relation-
ship to lead levels in water.  The pH level also affects the
formation or solubility of protective films on the inside of a
pipe.
     Alkalinity is a measure of a water's ability to neutralize
acids.  In potable water, alkalinity is mostly composed of
carbonates, which can neutralize acids, and bicarbonates, which
can neutralize bases as well as acids.  This property is called
"buffering," and can best be understood as resistance to change
in pH.  Alkalinity affects a water's ability to form a protective
coating of lead or calcium carbonate which is especially important
in reducing the dissolution of lead.  Water with low alkalinity
(i.e., under 60 mg/1 as CaCO3)-or very high alkalinity (> 150
mg/1) is generally corrosive.
     Hardness is caused predominantly by the presence of calcium
and magnesium ions and is expressed as the equivalent quantity of
calcium carbonate (CaCO3) in the water.  Hard waters are generally
less corrosive than soft waters if sufficient calcium ions and
alkalinity are present to form a protective calcium carbonate
lining on the pipe walls.  (A thin layer of CaCC>3 is desirable, as
it keeps the water from direct contact with the pipe and reduces
the chance of corrosion.  "Scaling" occurs when thick layers of
CaCO3 are deposited.  Although the pipe is then protected from
corrosion, excessive scaling can reduce the carrying capacity of
the system, reduce the efficiency of water heaters, clog water
meters, etc.)

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                                V-7





     Dissolved oxygen  (DO) is another substance that accepts the



electrons given up by  the corroding metal and so allows the cor-



rosion reactions to continue.  Oxygen also reacts with hydrogen



released by the cathode (see the following discussion on the



electrochemistry of corrosion) and with any ferrous iron ions.



Occasionally, oxygen may react with the metal surface to form a



protective coating of  the metal oxide.



     Chlorine lowers the pH of the water, making it potentially



more corrosive.  In addition, because chlorine is a strong oxidant,



it can increase a water's potential corrosivity.  A few studies



have also shown a difference in corrosion rates depending upon



whether the water is chlorinated or chloraminated.



    Chlorides and sulfates may cause metal pipes to pit by reacting



with the metals and creating soluble metal ions, thus preventing



the formation of protective metallic oxide films.  Chloride is



about three times more active in this than sulfate.  Higher total



dissolved solids (TDS) indicate a high ion concentration in the



water, increasing conductivity, which in turn increases the



water's ability to complete the electrochemical circuit and to



conduct a corrosive current.



     Other factors include the presence of hydrogen sulfide



(generally accelerates corrosion),  silicates and phosphates



(both of which can form protective  films), and natural color and



organic matter (which can either inhibit or encourage corrosion,



depending upon other characteristics).

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                                V-8

     BIOLOGICAL CHARACTERISTICS;  Both aerobic and anaerobic
bacteria can induce corrosion locally, and many organisms form
precipitates with iron.

V.A.2.  The Electrochemistry of Corrosivity
     Generally, metals are most stable in their natural form,
i.e., the form in which they occur in native ores and from which
they are extracted in processing.  The tendency of a metal to
return to its natural state (called "activity") is the primary
cause of corrosion.  Some metals are more active than others and
more easily enter into solution as ions or form various compounds.
Zinc, iron and lead are more active than, for example, copper or
stainless steel.
     The process by which metals corrode in water is electro-
chemical:  when a metal enters a solution as an ion or reacts in
water with another element to form a compound, electrons will flow
from certain areas on  the metal's surface to other areas through
the metal.  An anode is that part of the metal surface that  is
corroded and from which electric current flows through the metal
to the other electrode.  The cathode  is the metal surface from
which current  leaves the metal  and returns to the anode through
the solution.  This completes the circuit.  All water solutions
will conduct a current, a property measured by "conductivity."
The anode and  cathode  areas may  be right next to  each other  or
in different areas of  the pipe,  and  they can  set  up a current  in
the same metal or  between two different but connected metals.

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                                 V-9
V.A.3.   Types  of  Corrosion
      There  are many  types of  corrosion, which  can  be  either  uniform
or  non-uniform.   Uniform corrosion results  in  an equal  amount  of
material being lost  over an entire pipe surface; except in extreme
cases,  the  loss is often so minor that the  service life of the
pipe  is  not adversely effected.  On  the other  hand, non-uniform
corrosion attacks smaller, localized areas  of  the  pipe,  causing
holes,  restricted flow, or structural failures.  Non-uniform
corrosion is a serious problem.
      There  are five  basic types  of corrosion.  Galvanic  corrosion
occurs when two different metals or  alloys  come in contact with
each  other  or  are in the same environment (e.g., water).  This
usually  occurs at plumbing joints and connections.  Due  to the
differences  in their activity, the more active metal  corrodes.
Galvanic corrosion is common  in household plumbing where different
types of metals are  used, for instance, copper pipes  are joined
to galvanized  iron pipe or copper pipes are joined together  by
lead/tin solder.
     Pitting is a damaging, localized, non-uniform corrosion that
forms pits  or  holes  in the pipe surface.   It actually takes  very
little metal loss to cause a hole in a pipe wall,  and failure can
be rapid.  Pitting is frequently caused by  ions of a more-active
metal plating  out on the pipe surface.
     Tuberculation occurs when pitting corrosion products build
up at the anode next to the pit.
     Erosion corrosion (or abrasion)  mechanically  removes
protective films,  such as metal oxides and CaCC>3,  which serve as

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                                V-10

protective barriers against corrosive attacks.  Generally, it
results from high flow velocities, turbulence, changes in flow
direction, and/or the abrasive action of suspended materials.
     Biological corrosion results from a reaction between the
pipe material and the by-products of organisms such as bacteria.
     Dealloying or selective leaching is the preferential removal
of one or more metals from an alloy in a corrosive medium.

V.A.4.  Corrosion Indices
     Several indices have been developed to estimate the corrosion
potential of specific waters, but because they generally measure
the tendency of a specific water to form a protective coating of
calcium carbonate, none of these has been entirely successful in
predicting whether or not a water is actually corrosive  (Larson,
1975; Hoyt et al., 1979; AWWA-DVGW, 1985; etc).  The three most
commonly used indices (the Langelier Saturation Index, the Aggres-
sive Index, and the Ryznar Stability Index) consider calcium,
alkalinity, and pH as parameters to determine the corrosive
tendency of the water.  However, corrosivity  is a complicated and
interrelated function of these  three characteristics and many
others, and each parameter may  independently  affect the  corrosive
tendencies of the water.  Consequently,  some  water may be very
corrosive even though the measured  indexes  indicate relatively
non-corrosive conditions, or vice versa.  It  is generally agreed
that  these  indexes are  applicable only  within a limited  pH  range,
are dependent upon the  presence of  calcium  and alkalinity,  and
are most  appropriate  for the materials  for  which  the  index  was

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                                V-ll

developed;  they  are weakest  with  waters  of  relatively low alka-
linity and  calcium.

     The Langelier Saturation  Index  (LSI) or  Langelier Index  (LI),
developed in 1936, is one of the  first and  most  widely used;  it
expresses the potential of the water  to  either dissolve or pre-
cipitate calcium carbonate.  The  LSI  is  defined  as  the difference
between the measured pH of the water  and the  pH  at  which CaCC>3
would be at saturation concentration.  The  saturation value of the
water with  respect to CaCC>3  depends on its  pH, calcium ion con-
centration, alkalinity, temperature,  and total dissolved solids,
such as chlorides and sulfates; but the  LSI focuses particularly
on the effect of pH upon the solubility  of  CaCC>3.   A  positive LSI
value indicates  over-saturation and- a negative value  indicates an
undersaturation  of CaCC>3; a  value of  zero indicates equilibrium.
In other words,  a positive LSI indicates a  tendency for the water
to deposit a protective CaCC>3 layer on the  pipe, and  hence impede
corrosion.  Negative values  indicate  a water's tendency to dissolve
CaC03 from the pipe's interior and, thus, a tendency  to be aggres-
sive to the pipe.  The index is directional only, not  quantitative.
     The Aggressive Index (AI) is a simplified version of  the
LSI developed specifically for asbestos  pipes.   It  assumes .typical
values for total dissolved solids and for temperature.   The AI is
nearly interchangeable with the LSI for  most practical  purposes.
     Another common measure  is the Ryznar Stability Index  (RSI),
which uses the same parameters as the LSI.  Other corrosion indices
include the Larson, (McCauley) Driving Force, and the  Riddick
Corrosion Index.

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                                V-12


V.A.5.  Plumbosolvency and Other Factors Determining
        Lead Levels in Drinking Water

     Chapter II contains a more detailed discussion of the potential

contamination of drinking water by lead, the sources of that

contamination, and potential human exposure resulting from it.

This section briefly summarizes the major factors responsible

for the contamination of drinking water by lead.

     The lead used in service pipes or as part of lead/tin solder

is designed to be structurally relatively resistant to corrosion.

In addition, the corrosion rate can be decreased by a relatively

insoluble coating that forms on the surface of the metal.  However,

the combination of copper piping with tin/lead solder found in

most residences produces galvanic corrosion that can yield lead

levels one to two orders-of-magnitude higher than expected from

the composition of the water alone.  Many studies found that  lead

solder, especially newly-applied solder, used with copper household

pipes was sufficient to raise lead  levels above the current MCL,

even with relatively non-corrosive waters.

     With lead solder, the age of the solder is the single most

important variable affecting solubility.  As an example, Sharrett

et al.  (1982a), studying Seattle — a city with few lead pipes —

found that the age of the house  (a  proxy measure for the age  of

the plumbing materials, including solder) was the dominant factor

for predicting the concentration of lead in the tap water.  In

homes that were newer than five years old, with copper pipes, the

median  lead concentration for standing water was 31 ug/1 versus

4.4 ug/1  in older  homes.  The median lead level was 74 ug/1 in

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                                V-13

 homes built within the previous 18 months.  New solder will leach
 lead even in relatively non-corrosive water —'• whether naturally
 exhibiting low corrosivity or treated — and it can continue to
, leach significant amounts for up to five years.
      Two other factors will affect the rate of lead leaching
 from lead-soldered joints: the surface area of the lead/tin solder
 at the joints and the number of joints per length of pipe.
      The duration of contact need not be long.   Britton and
 Richards (1981)  have shown that, with corrosive water, lead
 levels in systems with copper plumbing joined with lead solder
 could rise above 100 ug/1 within 40 minutes of-contact.  Oliphant
 (1983)  has presented evidence that these conditions can produce
 lead levels one  to two orders-of-magnitude higher than expected
 from equilibrium solubility calculations.
      Several  characteristics of lead piping,  mentioned in decreas-
 ing order of  significance, also influence  lead  levels  in drinking
 water.   The length of the lead pipe,  in both  the  home  and the
 supply  lines,  can have a  positive  association with lead levels  as
 can the  position of  the lead pipe.   The ratio of  the surface
 area of  lead  exposed  to the  water  volume contained is  another
 important variable.   The  age of  the dwelling  and  the percentage
 of.lead  piping in both the service  mains and  within the residence
 were also relevant factors in  determining  lead  levels.   The
 number of occupants of the dwelling is  inversely proportional
 to  lead  levels,  probably  because fewer  occupants mean  the  water
 will, on  average,  remain  in  the pipes longer  (Department of the
 Environment, 1977; Pocock, 1980).

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                               V-14

     Lead can also leach from copper pipes themselves (Herrera et
al., 1981).  Specifications for copper pipes usually limit only
copper and phosphorus, and copper used for non-drinking water
applications is permitted to contain some lead.  Copper pipe
manufacturers have indicated that copper tubing for water is
made from the recycled copper products which could result
in the introduction of lead impurities (Herrera et al., 1981).
Although not common, lead impurities can also occur in galvanized
pipes and from stabilizers used in plastic pipes.
     Lead is also used in the production of brass and bronze.
Brass is a copper-zinc alloy, which can contain up to 12 percent
lead, and bronze is a copper-tin alloy, which can contain up  to
15 percent lead (U.S. EPA, 1982b).  Both are relatively corrosion
resistant, although several studies document lead leaching  from
bronze and brass fixtures.  Additional analysis of the leaching
of  lead  from these and other materials is needed.
     With  even mildly aggressive water,  any  amount of  lead  anywhere
in  the distribution system or household  will contribute lead  to
the  drinking water.  Overall, the  degree of  corrosivity,  the
length of  time  in  the pipe,  the  total  amount of  lead  in the plumb-
ing system and  the newness of the  plumbing  are the  chief  determin-
ants of  lead concentrations.
      In  general, with relatively corrosive  waters,  lead  levels in
 'first draw1 water can  be several  times  higher than in 'running1
 samples.  With  aggressive waters and new solder,  however,  first-
draw samples  can be  an  order-of-magnitude or more greater.

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                                V-15

 V'B»   Damage to Public Water Systems from Internal Corrosion
      Because lead contamination of drinking water occurs most often
 as a  result of the corrosive action of water upon the materials of
 the public  and private plumbing systems,  strategies to mitigate
 this  contamination will have to include corrosion control efforts.
 Corrosion in water supply  distribution systems  has economic  impacts
 as well  as  potentially creating health hazards.   It also can affect
 the aesthetic quality  of the water.   The  corrosion rate within a
 specific water system  is a function of the  character of the
 water, the  materials used  in the distribution system,  and of flow
 conditions.   But  notwithstanding the local  differences,  corrosion
 is a  universal problem:  corrosion occurs with  all metals currently
 used  in  plumbing  equipment and  construction, and  also  with asbestos-
 cement and  cement pipes.   Corrosion  impartially destroys  the
 distribution  system mains,  service  lines and private household
 plumbing; reduces the  flow .capacity  and increases  operating  costs
 throughout  the distribution  system;  and causes water loss through
 leaks and pipe  breaks.
     Corrosion  control  treatment will  produce substantial  benefits
 in  the form of  reduced  damage to public and private plumbing
 systems, as well  as reducing exposure  to lead which will  produce
 the health benefits described in Chapters III and  IV.

V.B.I.  Occurrence of Corrosive Water  in the United States
     Data on the  extent of aggressive water in the United States
are incomplete.  The most commonly held profile of the corrosivity
of U.S. drinking water relies on data on 600 public supply systems

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                                V-16

collected in 1962 by the U.S. Geological Survey (Durfor and
Becker, 1964a).  That study identified the Northeast, Southeast
and Northwest parts of the country as having relatively soft and
aggressive waters.*  Of the 26 states in those regions, 17 had
very soft water  (under 60 mg/1 as CaCO3):  Alabama, Connecticut,
Delaware, Georgia, Maine, Maryland, Massachusetts, Mississippi,
New Hampshire, New York, North Carolina, Oregon, Rhode Island,
South Carolina,  Vermont, Virginia, and Washington.   In 1980,
these states  had a combined population of  67.7 million people.
Figure V-l presents  the USGS  state findings.
     Also during the early 1960s, the U.S. Geological  Survey
conducted a survey of  the aggressiveness of  public water  supplies
in the 100  largest  cities in  the  country  (Durfor  and Becker,  1964b)
The  profile of  water corrosivity  in  this  study correlated fairly
well with  the state  study:   the  Northeast, Southeast,  and North-
west are most at risk  of  very soft  water.
      In  1974  and 1975, the  National  Center for Health  Statistics
 (NCHS)  conducted an extensive health examination  survey  of 4,200
 randomly selected  individuals representing 3,834  households in 35
 geographic areas across the country.  This was called  the National
 Health and Nutrition Examination Survey, augmentation survey, or
 HANES I, augmentation survey.  For each geographic area, the
 Bureau of Census selected 120 individuals to provide a "represen-
 tative" sample of the U.S.  population.  EPA participated in this
 *  While these studies present "average" data on water by state,
    it should be noted that water  (parameters and quality) varies
    significantly within states, as well.

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                          V-17
FIGURE V-l.  1962 U.S. Geological  Survey of Water
                                                            I
                                                             o
                                                            •r-
                                                            I
                                                             0)
                                                               s
§
I
 •
o

-------
                                V-18


survey to assess the role of drinking water quality and cardio-

vascular disease.  As part of this survey, the NCHS collected

a 1-quart "grab" sample of water from the kitchen faucet of each

participant, which was sent to EPA for analysis.

     Several studies have presented the data from this survey;

unfortunately, the results differ from study to study, and the

entire data set  is currently being re-analyzed at the University

of Pittsburgh.   One study (Greathouse and Osborne, 1980) indicates

that about one-third of the U.S. population is exposed to very

soft water (i.e., under 60 mg/1 as CaCO^) and that the median

U.S. drinking water is about 91 mg/l-CaCOs.  Another paper

(Greathouse and  Craun, 1978) presents mean concentrations at

119 mg/1.  A third study, Millette et al.  (1979), presented the

following distribution of aggressive water provided by' utilities

(using the Aggressive Index as  a measurement):

         16.5% of utilities had  highly aggressive water
                                (i.e. , AI £ 10.0) ,

         52% of  utilities  had moderately  aggressive water
                              (i.e. , AI =  10.0-11.9) ,

         31.5% of utilities had  non-aggressive water
                                (i.e. , AI J> 12.0) .

No results were presented by Millette on the  distribution  of

population  served  by  those utilities.  However,  if  the  average

water system  serves  3,650 people,  this distribution  suggests

 that 36  million people  are  exposed to very aggressive water and

 another  114 million people  are  exposed  to moderately aggressive

 water.

      Hudson and Gilcreas (1976),  basing  their analysis upon the

 U.S. Geological Survey data,  estimated  that  half of the water

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                                 V-19


 distributed in the U.S. is naturally corrosive, and is either

 untreated or,  for whatever reason(s), the treatments are not

 achieving chemical stability.   While the specific data they

 evaluate are related to the 100 largest cities (Durfor and Becker,

 1964b),  they assumed that larger systems generally provide better

 water than smaller systems.  Hudson and Gilcreas  then extrapolated

 linearly to the rest of the country.

      In  1979,  the A/C Pipe Producers Association  commissioned the

 Midwest  Research Institute (MRI)  to survey the occurrence,  economic

 implications and health effects associated with aggressive  waters

 in public water supply systems.   MRI  surveyed  more than  three-

 quarters  of the largest (i.e.,  serving  over 50,000 people)  public

 drinking  water systems in  the country and  about 10 percent  of the

 medium-size (serving  10,000-50,000)  systems.   Their results

 (using the  Langelier  Saturation  Index)  are extremely close  to

 those of  Millette  et  al.:*

        16%  of  utilities surveyed had highly aggressive waters
                                      (i.e. , LSI  <  -2.0) ,-

        51,5% of utilities surveyed had moderately  aggressive waters
                                      (i.e., -2.0  <  LSI < 0.0),

        32.5% of utilities surveyed had non-aggressive waters
                                      (i.e. , LSI  >  0.0).

They estimated  the population exposed only  for  the  utilities

they sampled; they did not extrapolate to  the rest  of the country,

or attempt  to draw a national profile from  their data.  However,

over 171.1 million people are served by medium and  large systems.
*  The MRI categories using the LSI correspond directly to
   Millette et al.'s, who used the AI.

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                               V-20



     Also in 1979,  Energy and Environmental Analysis (EEA),

using internal data from 1970, estimated that about 27 percent of

the U.S. population or 55 million people in 1970 were exposed to

very soft water.  This includes most of the population in the

northeastern, southeastern and western states.  While EEA did not

cite the source of their data, their map of soft water areas is

very similar to the 1962 U.S. Geological Survey.

     In Patterson's 1981 analysis using 1978 data from Culligan

dealerships throughout the country,* 7 states  (Alabama, Connecticut,

Mississippi, North Carolina,  Oregon, Rhode  Island, and South

Carolina) had soft water, i.e., under 60 mg/1  as CaCO3, with a

combined population in these  states of 22.1 million people  (1980

Census).  This  is  a low  estimate  of soft water occurrence because

the  data come from a  company  providing water-softening services

and  represent people  with harder-than-average  water?  indeed, the

average water hardness in the Culligan  data is significantly

higher than other  data.**   Notwithstanding this bias  in  the data,

the  profile of  the country  presented  by these data  support  the

U.S. Geological Survey map  of hard and soft water areas  in  the


 country.


 V.B.2.  Corrosion Damage

      Corrosion can take  place at the treatment plant, throughout

 the distribution system, and in household plumbing, and it  has

 many effects that cost utilities and consumers money.  Corrosion

 results in pipes breaking,  damage to meters and storage facilities,
 *   This data set is described in Chapter II.  The use of company
     names and the presentation of related data does not constitute
     endorsement of these services.

 **  This issue is discussed in Section II.B.I., above.

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                                   V-21


 water loss, excess repair and replacement of equipment, water

 damage from leaks, increased pumping costs due to the reduced

 hydraulic efficiency of corroded or partially blocked pipes, .loss

 of service pressure, and increased operating costs associated

 with all of these effects.  In addition, consumers suffer damage

 to private hot water heaters, radiators, and faucets.  Corrosion

 products also retard heat transfer for heating or cooling water,

 increasing both water use and operating costs.

      EPA has determined (1977)  that,  as an upper limit,  as much

 as half  the water leaving a  treatment plant may be lost  before

 ever reaching the consumer.   More conservatively,  the National

 Science  Foundation has estimated  that,  nationally,  15 percent

 of the water distributed is  lost.  Of course, not  all of this

 loss results from corrosive  water; some is  due  to  accidents

 or other  naturally occurring events.  MRI  (1979) calculated

 that 38 percent  of all  water loss  or  6  percent  of  total  water

 distribution is  lost  due to  corrosion from  aggressive waters.

      MRI's  survey  of  public  water  utilities  indicated that

 corrosion-related  repairs  in utilities  with  non-aggressive water

 were  about  62 percent of those in  utilities distributing relatively

 aggressive water.  Data  from other studies show that  reducing the

 corrosivity of the water could -reduce corrosion damage rates by

 at least 20 percent (Bennett et al.,  1979, cited in Ryder, 1980)

 or even 30-75 percent (Dangel, 1975;  Kennedy Engineers, 1978).

These surveys also show that pipe and equipment replacement and

 repair due to scaling, leakage or breakage* is the major economic
  Delaying the first break is important because while the
  probability of a break increases with age, once a break has
  occurred, the probability of another one is many times higher.

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                               V-22


effect of corrosion in distribution systems and that within this

category, pipe replacement is the primary maintenance item.

     Studies that present monetary estimates of corrosion

damage have generally focused upon either the cost to the

utility or the cost to the private residence owner; few have

done both.  Those studies that have tried to include all the

costs of corrosion damage have, by and large, covered smaller

geographic areas — a city or metropolitan area, typically.


V.B.3.  Estimating the Annual Costs of Corrosive Water

     Projections of the economic  impact of corrosive water

evidence a wide range of  factors  of concern, assumptions and

methodologies, producing, of course, a wide range  of "costs."

However,  including all of the components  of the problem and

converting costs to comparable-year estimates, the assumptions

and methodologies  in  the  different studies produce a much  nar-

rower range of cost estimates than seems  likely from an  initial

review  of  the  literature.*   The  factors  that must  be considered

in calculating the annual benefits of  reducing corrosivity include

the percentage of  corrosion  damage that  is  avoidable by  water

treatment,  the relative  damage  to public  and private plumbing

systems, total annual estimates  of corrosion damage, and the

occurrence of  corrosive  water  in the  U.S.  For comparability, we

have  calculated  per capita  estimates  and converted all costs to

 1985  dollars  using fixed-weighted price  indexes  from the 1986

Economic Report  of the President.
 *  This is all the more surprising because each of the "averages"
    (costs, damages, water characteristics, etc.) is the mean of
    a distribution of rather large-range values.

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                              V-23


      All water is corrosive to some degree.   Estimates of the

 incremental damage from particularly corrosive water and, hence,

 the potential benefits of corrosivity control treatment vary.

 Several studies of the highly aggressive water in Seattle,  Washington

 (both pre-treatment:  e.g.,  Kennedy Engineers, 1973 and 1978;

 Dangel, 1975;  and post-treatment,  e.g.,  Courchene and Hoyt,

 1985)  suggest that water treatment could reduce corrosivity

 damage by 30-75 percent,* or  even  more (AWWA-DVGW, 1985).

      Hudson and Gilcreas (1976)  assumed  that  corrosive water

 doubles natural deterioration rates,  and Kennedy Engineers  (1978)

 used  a 50 percent point  estimate of  avoidable damage  from corrosion.

 EEA (1979)  and  MRI  (1979) took a conservatively low point-estimate

 (38 percent)  from the  range presented  in the  earlier  Seattle

 studies;  similarly, Kirmeyer  and Logsdon (1983)  posit  that treat-

 ment can  reduce corrosivity by 40  percent.  Even more  conserva-

 tively, Ryder  (1980) projected that savings from corrosion control

 would  be  25 percent of the total,  and Bennett  et al.   (1979,

 cited  in  Ryder,  1980) estimated that 20  percent  of water supply

 corrosion costs were avoidable.

     Estimates  of the proportion of total corrosion damage

 (maintenance and capital expenses) borne by the private sector**
    Kennedy Engineers suggests that although corrosion damage can
    be reduced by 30-75 percent, costs can only be reduced by
    15-50 percent.   This distinction is also made in Internal
    Corrosion of Water Distribution Systems.  (AWWA-DVGW,  1985).

**  Of course, costs incurred by utilities are eventually  passed
    on to consumers.  However, by private sector costs we  mean
    those incurred  directly by owners of buildings,  and not by
    the utility.                                             *

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                             V-24

(primarily homeowners, but also building owners) range from "fully
half" (EPA, 1977) to 95 percent (e.g., Dangel, 1975; Ryder,
1980).*  Consumer costs are probably higher than distribution
costs for several reasons.
  o  Residential piping is often composed of copper or
     galvanized steel piping joined by brass fittings or
     lead/tin solder; combinations of dissimilar metals are
     particularly vulnerable to galvanic corrosion.
  o  Water used  in the home is often heated, increasing its
     corrosive potential.
  o  The materials used in residential plumbing are often  less
     resistant to corrosion and  less well-protected than the
     materials used  in distribution systems  (AWWA  Committee
     Report,  1984).
  o  Piping  in residences  is typically smaller  than service
     mains and flow  rates  are  more variable  (both  higher and
     lower),  exacerbating'many physical  characteristics affecting
     corrosion rates.
     Three studies  set out to  calculate  only the costs borne
 by  the water utility.  Bennett et al.  (1979, cited in Ryder,  1980)
 used 1975  data  from the  National Bureau  of Standards, which  esti-
 mated  that annual corrosion costs to  the overall U.S. economy were
 $70 billion,  of  which annual water supply corrosion costs  for
     In general, the highest estimates of the proportion of damage
     borne by the private sector are based upon data from Seattle •
     a city with a relatively new and corrosion-resistant distribu-
     tion system.  Older cities with less well-protected systems
     can incur a higher proportion of the total damage, and the
     total costs will be higher.

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                              V-25


 distribution systems were $700 million ($1,693.9 million in 1985

 dollars).  That study assumed that 20 percent of corrosion damage

 is avoidable through water treatment and estimated the annual

 benefits to utilities of reducing corrosivity at $1.88 per capita

 in 1985 dollars.   Hudson and Gilcreas (1976)  estimated annual

 savings of $375 million ($782.3 million in 1985 dollars)  to com-

 munity and other public water supplies from treatment to  reduce

 corrosivity;  their estimate  assumed that  aggressive water doubles

 the natural deterioration rate,  decreasing distribution capacity

 by 2 percent  annually,  instead of one percent.   The per capita

 annual estimate calculated from this  study is $4.34 in 1985

 dollars,  but  it does  not  include all  increased  operating  costs

 from corrosion  damage.  The  third study of utilities,  Kennedy

 Engineers,  1973  (cited  in  Anderson and  Berry,  1981),  estimated the

 annual  per  capita  damage  from  Seattle's highly  corrosive  water at

 $2.21  ($5.57  in 1985  dollars).   Assuming  that 30 percent  of those

 damages were  avoidable  costs,  this  yields  annual benefits of $1.67

 per  capita  for  avoided  damage  to  utility  systems.

     If utility costs are  half of private  costs,* these three

 annual per  capita estimates of avoidable damage to  utilities

 (in  increasing order, $1.67,  $1.88  and $4.34, in 1985 dollars)

would yield total annual per capita benefits of $5.01, $5.64 and

$13.02 (1985 dollars) for reducing corrosivity.
*  That is,
      1)  total costs of corrosion damage = cost to utilities and
                  cost to private sector,
         and cost to utilities = 1/2 cost to private sector,

      2)  benefits of corrosion control = avoidable damage
                  (% decrease in damage) x total costs of corrosion,

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                             V-26

     Two studies (Kennedy Engineers, 1978; and Kirmeyer and
Logsdon, 1983) calculated the savings that would accrue to
private residence owners from treatment for aggressive water.
Kennedy Engineers, studying Seattle, estimated that the cost
of corrosivity damage could be reduced by 20 percent, and
calculated that owners would save $7.50 per year per residential
unit ($13.57  in 1985 dollars) if Seattle's highly aggressive
water was treated.  Using demographic data in the article, this
yields  annual per capita benefits of $6.17.  Kirmeyer and
Logsdon, using a  'typical' situation, assumed that corrosivity
control could reduce damage by 40 percent, yielding present
value benefits of $244 per unit  ($292.59  in  1985 dollars)  over
the  remaining life of the plumbing.  Using data  from the  article
and  the AWWA, this yields annual per capita  benefits of $9.44
(1985 dollars).   If private  costs are  two-thirds of total
costs  (i.e.,  double the  costs — or benefits —  to utilities),
these  two  per capita  annual  estimates  of  benefits  to residential
owners  ($6.17 and $9.44,  in  1985 dollars)  would  yield  total
avoidable  corrosion damage  benefits of $9.26 and $14.16 per
capita per year,  in  1985 dollars.
      Finally, two other studies,  Energy and  Environmental Analysis
 (1979)  and Ryder (1980), estimated  total savings from treating
water to reduce its  corrosion potential.   EEA,  using data from
Dangel (1975) and Kennedy Engineers (1973),  considered pipe damage
 to both the public and private sectors and calculated potential
 annual savings  of $2.67 per capita ($4.54 in 1985 dollars).   This

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                               V-27


 is  an admitted underestimate because they did not include total

 increased  operating costs  (to either the  public  or private sector),

 damage to  residential  hot  water  heaters or utility equipment other

 than  pipes,  etc.,  and  they assumed that residential damage rates

 are equal  to utility rates;  their  assumed corrosion rate  is also

 lower than other  studies.   Ryder,  using data  collected while he was

 associated with Kennedy Engineers,  calculated total annual corro-

 sion  damage  in Seattle at  $7.4 million ($11.7 million in  1985

 dollars),* of  which  25 percent could  be avoided  by water  treatment;

 this  yields  potential benefits of  $5.84 per person per year

 (1985  dollars) from  control  of Seattle's  highly  corrosive  water.

      For comparison, Mullen  and Ritter (1980)  published results on

 efforts by the Middlesex Water Company in Woodbridge, New  Jersey,

 to reduce  damage to  their unlined cast iron water  mains from

 their  soft and aggressive water.  Those treatment  efforts  were

 rewarded by  reductions in corrosion rates of  70-80  percent,

 averaged over a 5-6 year period.  Alternatively, Hahin (1978)

 assessed corrosion damage as a function of total operating

expenses.   His analysis of four Air Force and  three Army bases

showed that corrosion costs averaged 8-25  percent of total annual

operating costs over a 10-year period.
  This is also somewhat of an underestimate (and Ryder presented
  it as such)  because it does not include costs to the suburban
  water agencies who buy and use Seattle's water, the costs of
  deterioration of copper pipe, or the costs associated with water
  conditioning or treatment to minimize corrosion in industrial and
  institutional buildings.  Ryder estimates that the total cost
  probably exceeds $10 million ($15.8 million in 1985 dollars).
  Because our  costs are all per capita, we would then have to
  divide this  larger figure by the population of the entire
  metropolitan area.

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                               V-28

     We have not used cost estimates from two studies:  MRI (1979)
and Anderson and Berry (1981).  In the MRI study, the self-reported
expenditures attributable to corrosion totalled $8.3 million
annually for the utilities surveyed.  (Note that this is not a
national estimate and that it is an estimate of expenditures, not
damage.)  The largest estimate in that survey was much higher
than any of the others, indicating either more serious problems
for that utility or that they misinterpreted the question.
Eliminating that utility drops the estimated costs to $3 million
annually for the surveyed utilities.  The corresponding per
capita  costs are $1.15 (including all the utilities) or $0.42
(omitting the outlier); converting to 1985 dollars yields  $1.96
and $0.71,  respectively.  However, the question  asked in the
survey, "What are your annual  costs due  to corrosion?", could
easily  lead to  an underestimate  of real  costs,  for  several reasons.
First,  the  utilities  reported  only on their  expenditures and not
on those incurred by  consumers (which could  be  much greater).
Second, the utilities reported only on  their expenditures  and
expenditures  are  a  poor  estimate of damage;  the utilities  did
not quantify  the  damage  that was occurring  (for example,  leaking
but not broken  pipes) but for which they were not (yet)  paying
 (specifically identified)  money.  Finally,  it is unclear from
 the data whether  any of  the utilities identified increased
 operating costs associated with corrosive water (for example,
 water loss from leaks or the increased energy costs of pumping
 water through pipes partially clogged with corrosion by-products)
 or the proportion of regular maintenance costs  (e.g. leaks and
 breaks) that are attributable to corrosion damage.  From  the

-------
                                V-29

 information presented, it is likely that only major capital
 expenditures were included.
      Anderson and Berry (1981) evaluated the costs and benefits
 of regulating corrosive water.  They used the arithmetic mean
 ($2.37 per capita) of the EEA and Hudson and Gilcreas studies
 cited above, $2.67 and $2.08 per capita respectively, as their
 estimate of the materials benefits of reducing the corrosivity
 of drinking water.  However, none of the monetized estimates
 in the Anderson and Berry article were first converted to same-
 year dollars,  so they are not comparable.   Furthermore,  the EEA
 estimate includes both private and distribution costs while the
 Hudson and Gilcreas  analysis considers only distribution costs;
 again,  the estimates are  not comparable.   Finally,  Anderson and
 Berry didn't estimate an  independent measure of benefit,  but
 relied  upon previous work.   Because  we have included  the  material
 they cite,  their analysis  offered no independent and  additional
 data.
      The range  of  estimated  benefits from  treatment to reduce
 the  corrosivity of water  is,  then, from $4.54  (the admitted  under-
 estimate in  EEA, 1979)  to $14.16  (Kirmeyer  and  Logsdon, 1983),
 both  in  1985 dollars, per person  per year.   Table V-l summarizes
 all the studies.

V*B'4*  Monetized Benefits of Reduced Corrosion Damage
     To calculate the annual benefits of reducing the damage
caused by corrosive water, we multiplied the number of exposed
people by the per capita estimate of corrosion damage.  All
costs are converted to 1985 dollars.

-------
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-------
                                V-31

      Estimates of the population at risk of exposure to corro-
 sive water in the U.S.  range from 22.1 million people (Patterson,
 1981)  to 75.4 million people (Greathouse and Osborne, 1980).   Of
 the available data,  we  have used the U.S.  Geological Survey data
 on the occurrence of soft water,   in 1980, there were 67.7  million
 people living in  areas  identified by USGS  as having  soft and
 aggressive water.*
      Assuming that these  people are served proportionately  by
 community and non-community water systems,
                            219
            67.7  million  x 240  million = 61.8  million

 people would  benefit from actions to reduce the  corrosivity of
 their  water.
     From Table V-l,  we have used $8.50 per capita as a  point
 estimate  of potential annual savings benefits- from water treatment
 to  reduce  corrosivity.  This is the  mid-point  of  the  estimates
 including  the EEA  underestimate  ($8.21) and excluding it ($8.82).
 Multiplied by the  potentially exposed  population  (61.8 million)
 yields  annual materials benefits  from  reduced  corrosivity of
 $525.5 million in  1985 dollars.
     For comparison,  estimates of average  corrosion treatment
 costs  range from under $1 per person per year  to  about $5 per
person per year.  The lowest estimates are  data collected from 18
cities  in six states  now known  (by EPA) to  be  treating their water
*  This may somewhat underestimate the real exposure to soft water
   because many people in hard water areas install water softeners.

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                               V-32

to reduce its corrosivity.  System size varies from 6,000 to
550,000.  Annual capital and operating costs for these cities
range from $0.26 per person per year to $1.28 per person per
year.  System size was not related to per capita cost.
     Another estimate, arguably an upper-bound estimate, is from
Applegate (1986).  This article presented post-treatment
requirements, options and associated costs for reverse osmosis
(RO)* product water.  RO waters are usually extremely corrosive,
with pH typically of 5.5-6.9 (Applegate, 1986).  Hardness and
alkalinity are typically low, also.  Applegate calculated average
costs for post-treatment of RO product waters for use in municipal
drinking water systems.  Assuming  100 gallons of water used per
person per day, his estimates yield annual capital and operating
costs for various processes ranging from $1.28 to $3.03 per person
per  year.
     The highest estimate of annual cost is  from EPA's cost
estimates  (DS-EPA,  1984a),  for treatment costs for small systems
(i.e.,  serving up to  1000 people).  The point estimate,  averaging
costs for pH  adjustment,  use of  corrosion  inhibitors, and  stabilizing
corrosive water,  is a  little over  $5  per person per  year.   The  range,
however,  is  quite wide and  highly  sensitive  to  system size.   In
some very  small  systems (i.e., serving  25-100 people),  costs  may
be many times higher.
     To be  conservative,  we used $3.80  as  the point  estimate  of
annual  per capita treatment costs.  This  is  the  arithmetic mid-
 *  Reverse osmosis is a technology used primarily for desalinizing
    sea or other brackish water.

-------
                              V-33

point of the technologies evaluated in US-EPA (1984a), adjusting
for number of systems and population served.  Multiplying by the
61.8 million people estimated to be receiving corrosive waters
produces an annual cost estimate of $234.8 million annually,
yielding a benefit-to-cost ratio of over 2:1 for materials
benefits, alone.  Because the point estimate for treatment costs
is probably overestimated, net benefits are probably under-
estimated.
     These benefits will not be affected by the 1986 Amendments
to the Safe Drinking Water Act, which prohibit the use of
materials containing lead in public water systems.  The estimates
in this chapter (both costs and benefits) are based upon the
extent of corrosive water in the country, not the population
exposed to lead in drinking water.

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                             REFERENCES


Agerty HA.  (1952) Lead poisoning in children. Med Clin North Am;
  36: 1587-97.

Abu-zeid HAH.  (1979) The water factor and mortality from ischemic
  heart disease:  A review and possible explanations for inconsistent
  findings.  Archives of Environmental Health; 34: 328-336.

Ainsworth RG, Bailey RJ, Commins BT, Packham RF, Wilson AL. (1977)
  Lead in drinking water,, Water Research Centre Technical Report 43;
  England.

Akers CJ, Fellows R. (1978) Review of the problem of lead in drink-
  ing water. Presented at 82nd annual conference of the Scottish
  Institute of Environmental Health; Scotland.

American Water Works Association (AWWA). (1984) Water Quality Divi-
  sion Committee report. Determining internal corrosion potential
  in water supply systems. JAWWA; p. 85-88.

American Water Works Association (AWWA). Research Foundation and
  DVGW - Forschungsstelle. (1985) Internal Corrosion of Water
  Distribution Systems, cooperative research report.  Printed by
  the AWWA Research Foundation.

Anderson G, et al. (1984) Development and application of methods
  for estimating:  effects of industrial emission controls on air
  quality impact of reactive pollutants. U.S. EPA July.

Anderson PA. (1984) Metal piping and joining materials and fittings.
  Presented at the Plumbing Materials and Drinking Water Quality
  Seminar.  Sponsored by EPA; Cincinnati, Ohio.

Anderson R, Berry D. (1981) Regulating corrosive water. Water
  Resources Research; 17(6):   1571-1577.

Angino EE.  (1979) Geochemistry in Relation to Cardiovascular Disease.
  National Academy of Sciences, Washington, DC.

Angle CR and Mclntire MS. (1982) Children,  the barometer of environ-
  mental lead. In:  Barness L (ed):  Advances in Pediatrics, Yearbook
  Medical Publishers, Inc., Chicago; p. 3-32.

Angle CR, .Mclntire MS,  Swanson MS,  Stohs SJ. (1982) Erythrocyte
  nucleotides in children - increased blood lead and cytidine
  triphosphate. Pediatric Research; 16: 331-4.

-------
                                -2-
Annest JL, Mahaffey KR, Cos DH, et al. (1982) Blood lead levels for
  persons 6 months - 74 years of age:  United States 1976-1980.
  National Center for Health Statistics,  Advanced Data no. 79.
Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG,
  Chronological trend in blood lead levels between 1976 and
  1980. New England Journal of Medicine; 308: 1373-7.
(1983)
Applegate LE.  (1986) Posttreatment of reverse osmosis product
  waters.  JAWWA; May: p. 59-65.

Aub JC, Fairhall LT, Minot AS, Reznikoff P, Hamilton A. (1926) Lead
  Poisoning in Baltimore, MD. The Williams and Wilkins Company
  (Medicine Monographs:  V.7.).

Aub JC.  (1935) The biochemical behavior of lead in the body. Journal
  of the American Medical Association; 104: 87-90.

The Australian Therapeutic Trial in Mild Hypertension: Report by
  the management committee. (1980) Lancet; 2: 1261-7.

Bailey RJ, Russell PF. (1981) Predicting drinking water lead levels.
  Environmental Technology Letters; 2: 57-66.

Baksi SN, Hughes MJ. (1982) Regional alterations of brain catechola-
  mines by lead ingestion in adult rats. Arch Toxicol; 50: 11-18.

Barltrop D. (1969) Transfer of lead to the human fetus. In: Barltrop
  and Burland (eds), Mineral Metabolism in Pediatrics.  Davis Co.,
  Philadelphia.

Barton JC, Conrad ME, Nuby S, Harrison L.  (1978) Effects of iron on
  the absorption and retention of lead. Journal of Laboratory and
  Clinical Medicine; 92: 536-47.

Battelle. (1982) Examination of the leaching of lead from 50 tin -
  50 lead soldered copper plumbing by simulated drinking waters.
  Topical Report; April.

Batuman V, Landy E, Maesaka JK, Wedeen RP. (1983) Contribution of
  lead to hypertension with renal impairment. New England Journal of
  Medicine; 309: 17-21.

Beattie AD, Moore MR, Goldberg A, et al. (1975) Role of chronic low-
  level lead exposure with aetiology of mental retardation.  The
  Lancet;  March: p. 589-592.

-------
                                -3-
Beevers DG, Erskine E, Robertson M, Beattie AD, Campbell
  BCf Goldberg A, Moore MR, Hawthorne VM. (1976) Blood-lead and
  hypertension. Lancet; 2(7975): 1-3.

Beevers DG, Cruickshank JK, Yeoman WB, Carter GF, Goldberg A,
  Moore MR. (1980) Blood-lead and cadmium in human hypertension.
  J Environ Pathol Toxicol; 4s 251-60.

Bellinger D, Leviton A, Needleman H, Nichols M, Rabinowitz M,
  Waternaux C. (1984) Early sensory-motor development and prenatal
  exposure to lead. Neurobehavioral Toxicology and Teratology;
  6:387-402.

Bellinger D, Leviton A, Needleman H, Rabinowitz M, Waternaux C.
  (1985) A longitudinal study of the developmental toxicity of
  low-level lead exposure in the prenatal and early postnatal
  periods. Paper presented at the Heavy Metals in the Environment
  Conference; Athens, Greece.

Bellinger D, Leviton A, Needleman HL, Rabinowitz M, Waternaux C.
  (1986a)  Low-level lead exposure and infant development in the
  first year.  Neuro-behav Toxicol Teratol; 8:  151-61.

Bellinger D, Leviton A, Needleman H, Rabinowitz M, Waternaux C.
  (1986b) Correlates of low-level lead exposure in urban children
  at 2 years of age. Pediatrics.

Benignus VA, Otto DA, Muller KE, Seiple KJ. (1981)  Effects of age
  and body lead burden on CNS function in young children:  II.
  EEC Spectra. Electroencephalog Clin Neurophysiol; 52: 240-8.

Betts PR, Astley R, Raine DN. (1973) Lead intoxication in children
  in Birmingham. British Medical Journal; 1(5850): 402-6.

Bhalla AK, Amento EP, Clemens T, Holick MF, Krane SM.  (1983) Specific
  high-affinity receptors for 1,25-dihydroxyvitamin 03 in human
  peripheral blood mononuclear cells:  presence in monocytes and
  induction in T lymphocytes following activation.  J Clin
  Endocrinol Metab; 57: 1308-10.

Billick IH, Curran AS, Shier DR. (1979) Analysis of pediatric blood
  lead levels  in New York City for 1970-1976. Environmental
  Health Perspectives; 31: 183-90.

-------
                                         -4-
         Billick  IH,  et  al.  (1982)  Predictions  of  pediatric  blood  lead  levels
           from gasoline consumption.  U.S.  Department  of  Housing and
           Urban  Development.

         Birden HH Jr, Calabrese  EJf  Stoddard A.  (1985) Lead dissolution  from
           soldered  joints.  JAWWA  November; p.  66-70.

         Blomquist G.  (1977) Valuation of  Life:  Implications of automobile
           seat belt  use.  Ph.D. Dissertation; University  of  Chicago.

         Bornschein RL.  (1986) Effects of  prenatal and postnatal lead
           exposure on fetal maturation and postnatal  growth.  Presented
           at  the Joint  EPA-EEC Conference on Lead and Neurotoxicity ;
           Edinburgh, Scotland; September.

         Brennan  MJW, Cantrill RC.  (1979)  y-Aminolevulinic acid is  a potent
           agonist for GABA auto  receptors. Nature;  280:  514-5.

         Britton  A/ Richards WN.  (1981)  Factors  influencing  plumbosolvency .
           Journal of the  Institute of Water Engineers and Scientists;
           July.

         Brookshire DS,  et al. (1986)  The  valuation  of aesthetic preferences.
           J Environ  Econ  Manag;  3: 325-46.

         Brown C.  (1980)  Equalizing differences  in the labor market.
           Quarterly  Journal of Economics;  94.

         Bryant EC.  (1966) Statistical Analyses  (2nd Edition).  McGraw Hill;
           New York.

         Bryce-Smith  D,  Deshpunde RR,  Hughes J, Waldron HA.  (1977)  Lead and
           cadmium levels  in still  births.  Lancet;  1:  1159.

         Bryce-Smith  D.  (1986) Environmental chemical  influences on behavior
           and mentation.  Chemical Society Review;  15:93-123.

         Budiansky S. (1981) Lead:  the debate goes on, but not  over science.
           Environmental Science  and  Technology; 15(3): 243-246.

         Bull  RJ, Stanaszek PM, O'Neill  J J , Lutkenhoff SD. (1975) Specificity
           of  the effects  of lead on  brain energy  metabolism for substrates
           donating a cytoplasmic reducing equivalent. Environmental Health
           Perspectives;  12: 89-95.
_

-------
                                 -5-
 Bull  RJ.  (1977)  Effects  of trace metals and their derivatives on
   the control  of brain energy metabolism.  Lee SD ed.,  Biochemical
   Effects of Environmental Pollutants.  Ann Arbor Science;  Ann
   Arbor,  Mi; p.  425-40.

 Bull  RJ,  Lutkenhoff SD,  MeCarty GE,  Miller RG.  (1979)  Delays  in
   the postnatal  increase of cerebral eytoehrome concentrations in
   lead-exposed rats.  Neuropharmaeology; 18: 83-92.

 Bull  RJ.  (1980)  Lead and energy metabolism. In: Singhal  PL, Thomas
   JA  (eds).  Lead Toxieity.  Urban and  Sehwarzenberg,  Inc.;
   Baltimore: p.  119-68.

 Bull  RJ,  MeCauley DT,  Tayler DH,  Crofton KM.  (1983)  The  effects of
   lead on the  developing central nervous system of  the rat.
   Neurotoxieology;  4(1):  1-17.

 Bureau of Food and Drug  Administration, Compliance  Program Report
   of  Findings, Total Diet Studies, 1973-1980  reports.

 Byers RK. (1959)  Lead poisoning,  review of the  literature  and
   report  on forty-five cases.  Pediatrics;  23: 585-603.

 Calabrese EJ,  Tuthill RW.  (1978)  Elevated  blood pressure levels
   and community  drinking water characteristics.  Journal of
   Environmental  Science  and Health;  A13 (10): 781-802.

-Cal.abrese E et al.  (ed).  (1985)  Inorganics in Drinking Water  and
   Cardiovascular Disease.   Princeton Scientific Press; Princeton,
   NJ.

 Carmichael NG, Winder C,  Lewis PD. (1981)  Dose  response  relation-
   ships during perinatal lead administration  in the  rat:  a model
   for the study  of lead  effects on brain development.  Toxicology;
   21:  117-128.

 Charney E, Kessler B,  Farfel M,  et al.   (1983)  Childhood lead
   poisoning.   A  controlled trial of  the effect  of dust-control
   measures on  blood lead levels.  New England  Journal of  Medicine;
   309:  1089-1093.

 Chesney RW, Rosen JF,  DeLuea HP.  (1983) Disorders of calcium
   metabolism in  children.  Chiumello, Sperling M (eds), Recent
   Progress in  Pediatric  Endocrinology.  Raven  Press;  New  York, NY;
   p.  5-24.

-------
                                -6-
Chin D, Karalekas PC. (1984) Lead product use survey of public
  water supply distribution systems throughout the U.S.  Pro-
  ceedings of:  Seminar on Plumbing Materials and Drinking Water
  Quality; Sponsored by US EPA; Cincinnati, Ohio; May  (appendix).

Chisolm JJ Jr, Harrison HE. (1956) The exposure of children to
  lead. Pediatrics; 18: 943-58.

Chisolm JJ Jr. (1968) The use of chelating agent in the treatment
  of acute and chronic lead intoxication in children. J Pediatr
  (St. Louis); 73: 1-38.

Chisolm JJ Jr, Barltrop D. (1979) Recognition and management of
  children with increased lead absorption. Arch Dis Child; 54:
  249-62.

Clark, ARL. (1977) Placental transfer of lead and its effects on
  the newborn. Postgrad. Med. J. 53: 674-678.

Cohen GJ, Ahrens WE. (1959) Chronic lead poisoning: a review of seven
  years' experience at the Children's Hospital, District of Columbia.
  J Pediatr (St Louis); 54: 271-84.

Comstock GW. (1979) Water hardness and cardiovascular disease.
  American Journal of Epidemiology; 110: 375-400.

Comstock GW. (1985) Water quality and cardiovascular disease: a
  review of recent studies in Canada and the US.  Paper presented at
  the International Symposium on Geochemistry and Health; London,
  England; April.

Conrad M, Barton J. (1978) Factors affecting the absorption and
  excretion of lead in the rat. J of Gastroenterology; 74: 731-740.

Cooper WC, Gaffey WR. (1974-1975) Mortality of lead workers. In:
  Cole JF (ed.) Proceedings of the 1974 Conference on Standards of
  Occupational Lead Exposure; J Occup Med; 17: 100-7.

Cooper WC. (1981) Mortality in employees of lead production facili-
  ties and lead battery plants, 1971-1975. In: Lynam Dr, Piantanida LG,
  Cole JF (eds.) (1978) Environmental Lead;  Proceedings of the Second
  International Symposium on Environmental Lead Research; Cincinnati,
  OH, December. Academic Press; New York; p. 111-143.

Council on Environmental Quality (1980) Environmental Quality - 1980.
  Government Printing Office, December.

Courchene JE,  Hoyt BP. (1985) The benefits of corrosion treatment
  in Seattle.   Presented at the California/Nevada Section of the
  AWWA Seminar on Water Quality and Treatment for Corrosion Con-
  trol; California.

-------
Crank J.  (1975) The Mathematics of Diffusion.  Clarendon Press;
  Oxford, England.

Craun GF, McCabe LG.  (1975) Problems associated with metals in
  drinking water. Journal of the American Water Works Association;
  67(11):593.

Crofton KM, Taylor DH, Bull RJ, Snulka DJ, Lutkenhoff SD. (1980)
  Developmental delays in exploration and locomotor activity in
  male rats exposed to low level lead. Life Science; 26: 823-31.

Dangel RA. (1975) Study of corrosion products in the Seattle water
  department distribution system, U.S. EPA report 670/2-75-036;
  Cincinnati, Ohio.

De Kort, WL, Verschoor MA, Wibowo AA, van Hemmen JJ. (1986) Occu-
  pational exposure to lead and blood pressure.  A study of 105
  workers.  Am J Ind Med.

De^la Burde B, Choate MS Jr. (1972) Does asymptomatic lead exposure
  in children have latent sequelae. Journal of Pediatrics; 81:
  1088-91.

De la Burde B, Choate MS Jr. (1975) Early asymptomatic lead exposure
  and development at school age. Journal of Pediatrics; 87: 638-42.

Delves HT. (1970) A micro-sampling method for the rapid determination
  of lead in blood by atomic absorption spectrophotometry. Analyst;
  431-3.

Department of the Environment.  (1977) Lead in Drinking Water:  A
  Survey in Great Britain. Pollution Paper 12; HM 50; London.

Dietrich KN, Krafft KM, Shukla R, Bornschein RL, Succop PA. (1986)
  The neurobehavioral effects of prenatal and early postnatal
  lead exposure. In Schroeder (ed): Toxic Substances and Mental
  Retardation, Neurobehavioral Toxicology and Teratology, AAMD
  Monography Series; Washington, DC.

Dingwall-Fordyce I, Lane RE. (1963) A follow-up study of lead
  workers.  Brit J of Ind Med;  20: 313-5.

Donald JM, Cutler MG, Moore MR.  (1986) Effects of lead in the labora-
  tory mouse. I. Influence of pregnancy upon absorption, retention,
  and tissue distribution of radio-labeled lead.  Environmental
  Research;  41: 420-431.

Donaldson W.  (1924) The action of water on service pipes.  Journal
  of the American Water Works Association;  11(5):  649.

-------
                                -8-
Dresner DL, Ibrahim NG, Mascarenhas BR, Levere RD. (1982)
  Modulation of bone marrow heme and protein synthesis by trace
  elements. Environ Res; 28: 55-66.

DRI. (1983 and 1984) The Data Resources Inc:  Review of the U.S.
  economy. Various issues; DRI; Lexington, MA.

Du Pont. (1986) Du Pont comments on the February 1986 draft docu-
  ment. Wilmington, Delaware. Available for inspection at:  US-EPA
  Central Docket Section; Washington, DC; Docket No. ECAO-CD-81-2
  IIA.E.C.3.6.

Durand D. (1971) Stable Chaos. General Learning Corporation;
  Morristown, NJ.

Durfor CN, Becker E. (1962) Chemical quality of public water
  supplies of the U.S. and Puerto Rico; Hydrologic Investigations
  Atlas HA-200; (1964a) U.S. Geological Survey.

Durfor CN, Becker E. (1972) Public water supplies of the 100 largest
  cities in the U.S.; Geological Survey Water-supply Paper 1812
  (1964b) U.S. GPO.

Edelstein S, Fullmer CS, Wasserman RH. (1984) Gastrointestinal
  absorption of lead in chicks:  involvement of the cholecalciferol
  endocrine system.  J Nutr; 114: 492-700.

Energy and Environmental Analysis (EEA). (1979) Health and corrosion
  impact of soft water. Prepared for the A/C Pipe Producers Associa-
  tion.

Ennis JM, Harrison HE. (1950) Treatment of lead encephalopathy
  with BAL (2,3-dimercaptopropanol). Pediatrics; 5: 853-68.

Erickson MM, Poklis A, Gantner GE, Dickinson AW, Hillman LS. (1983)
  Tissue mineral levels in victims of sudden infant death syndrome.
  I.  toxic metals - lead and cadmium. Pediatric Research; 17:
  784-99.

Ernhart CB, Landa B, Schell MB. (1981) Subclinical levels of lead
  and developmental deficits - a multi-variate follow-up reassess-
  ment.  Pediatrics 67: 911-919.

Ernhart CB, Wolf AW, Kennard MJ, Filipovich HF, Sokol RJ, Erhard P.
  (1985) Intrauterine lead exposure and the status of the neonate.
  Paper presented at the Heavy Metals in the Environment Conference;
  Athens, Greece.

Ernhart CB, Wolf AW, Kennard MJ, Erhard P, Filipovich HF, Sokol RJ.
  (1986).  Intrauterine exposure to low levels of lead: the status
  of the neonate.  Archives of Environmental Health.

Evis MJ, Kane KA, Moore MR, Parratt JR. (1985) The effects of chronic
  low lead treatment and hypertension on the severity of cardiac
  arrhythmias induced by coronary artery ligation in anesthestized
  rats.  Toxicol Appl Pharmacol 80: 235-242.

-------
                                -9-
Expert Committee on Trace Metal Essentiality. (1983) Independent
  peer review of selected studies by Drs. Irchgessner and Reichlmayr-
  Lias concerning the possible nutritional essentiality of lead:
  official report of findings and recommendations of an interdis-
  ciplinary expert review committee. Available for inspection at:
  U.S. Environmental Protection Agency, Environmental Criteria
  and Assessment Office; Research Triangle Park, NC.

Expert Committee on Pediatric Neurobehavioral Evaluations. (1983)
  Independent peer review of selected studies concerning neuro-
  behavioral effects of lead exposures in nominally asymptomatic
  children:  official report of findings and recommendations of an
  interdisciplinary expert review committee.  Available for inspec-
  tion at: U.S. Environmental Protection Agency, Environmental Cri-
  teria and Assessment Office,, Research Triangle Park, NC.

Fahim MS, Fahim Z, Hall DG. (1976) Effects of subtoxic lead levels
  on pregnant women in the state of Missouri. Res Commun Chemical
  Pathol Pharmacol; 13(2): 309.

Favalli L, Chiari MC, Piccinini F, Roza A. (1977) Experimental
  investigations on the contractions induced by lead in arterial
  smooth muscle.  Acta Pharmacol Toxicol; 41: 412-420.

Ferris B Jr. (1978) Health effects of exposure to low levels of
  regulated air pollutants. Journal of the Air Pollution Control
  Association; 28(5): 482.
Fisher RA. (1970) Statistical Methods for Research Workers.
  Press; New York.
   Hafner
Forbes FF. (1900) A very brief discussion of lead poisoning caused
  by water which has been drawn through lead service pipe. Journal
  of the New England Water Works Association; vol. 15.

Forthofer RN. (1983) Investigation of non-response bias in NHANES
  II. American Journal O'f Epidemiology.

Fouts PJ, Page IH. (1942) The effect of chronic lead poisoning on
  arterial blood pressure in dogs. American Heart Journal; 24:
  329-31.

Fowler BA. (1978) General subcellular effects of lead, mercury,
  cadmium, and arsenic. Environ Health Perspect; 22: 37-41.

Fowler BA, Kimmel CA, Woods JS, McConnell EE, Grant LD.  (1980)
  Chronic low-level lead toxicity in the rat: III. an integrated
  assessment of long-term toxicity with special reference to the
  kidney.  Toxicol Appl Pharmacol; 56: 59-77.
Freeman AM III.  (1982) Air and Water Pollution Control;
  Cost Assessment.   John Wiley and Sons; New York.
A Benefit-

-------
                                -10-
Preeman R.  (1965) Reversible myocarditis due to chronic lead
  poisoning in childhood. Arch Dis Child; 40: 389-93.

Gartside PS. (1985) NHANES II statistical overview and evaluation.
  Presented at:  Lead environmental health. Duke University; North
  Carolina.

Gerking S, Stanley L, Weirick W. (1983) An economic analysis of air
  pollution and health:  the case of St. Louis. Prepared for U.S.
  EPAr Office of Policy Analysis; July.

Glasson WA, Tuesday CS. (1970) Environ Sci Technol; 4: 37.

Goldberg AM, Meredith DA, Miller S, Moore MR, Thompson CG. (1978)
  Hepatic drug metabolism and heme biosynthesis in lead-poisoned
  rats.  British Journal of Pharmacology; 62: 529-36.

Goldman JM, Vander AJ, Mouw DR, Reiser J, Nicholls MG. (1981)
  Multiple short-term effects of lead on the renin-angiotension
  system. J Lab Clin Med 97: 251-263.

Govoni S, Lucchi L, Batlaini F, et al. (1980) Effects of chronic
  lead treatment affects dopaminergic control of prolactin secretion
  in rat pituitary. Toxicol Letters; 20: 237-241.
Goyer RA, Rhyne BC. (1973) Pathological effects of lead,
  Rev Exp Pathol; 12: 1-77.
Internal
Grant LD, Kimmel CA, West GL, et al. (1980) Chronic low-level lead
  toxicity in the rat II. Effects on postnatal physical and
  behavioral development. Toxicol Appl Pharmacol; 56: 42-58.

Greathouse DG, Craun GF. (1978) Cardiovascular disease study:
  occurrence of inorganics in household tap water and relationships
  to cardiovascular mortality rates. In:  DD Hemphill (ed), Trace
  Substances in Environmental Health - XII.; p. 31-39.

Greathouse DG, Osborne RH. (1980) Preliminary report on nationwide
  study of drinking water and cardiovascular diseases. J of Envir
  Path and Toxicol; 3: 65-76.

Gregory R, Jackson PJ. (1983) Reducing lead in drinking water.
  Water Research Centre; Regional Seminars May-June.

Gregory R, Jackson PJ. (1984) Central water treatment to reduce
  lead solubility. Paper presented at AWWA Annual Conference;
  June; Dallas, Texas.

Gross-Selbeck E, Gross-Selbeck M. (1981) Changes in operant behavior
  of rats exposed to lead at the accepted no-effect level. Clinical
  Toxicology; 18: 1247-56.

-------
                                 -11-
 Gunter EW,  et  al.  (1981)  Laboratory procedures  used  by  the  Clinical
   Chemistry Division,  Centers  for  Disease  Control, for  the  Second
   National  Health  and  Nutrition  Examination  Survey.   Centers  for
   Disease Control;  Atlanta,  GA.

 Hackney JD.  (1976)  Effects  of  atmospheric  pollutants  on human
   physiologic  function. Final  report;  U.S. EPA.

 Hahin  C.  (1978)  Predicting  the metallic  corrosion costs of  operating
   and  maintaining  buildings  and  utility  systems. Materials  Performance;
   September; p.  31-34.

 Harlan WR,  Landis  JR,  Sehmouder  RL,  et al. (1985) Relationship of
   blood lead and blood pressure  in  the adolescent and adult U.S.
   population.  Journal  of  the American  Medical Association;
   January 25.

 Harrison. Principles of Internal Medicine. Ninth Edition^

 Hartunian NS,  Smart CN, Thompson MS. (1981) The Incidence and
   Economic  Costs of Major Health Impairments. Lexington Books;
   Lexington, MA.

 Harvey P, Hamlin M, Kumar R. (1983)  The  Birmingham blood lead
   study.  Presented at: annual conference of the British Psychological
   Society,  Symposium on lead and health.  Available for inspection
   at:  U.S.  Environmental Protection  Agency, Environmental Criteria
   and  Assessment Office, Research Triangle Park, N.C.

 Hasselblad V.  (1981) Modeling dose response relations for health
   effects data.  Environmetrics 81: Selected Papers, SIAM.

 Heintz  HT, Hershaft A, Horak GC. (1976)  National Damages of Air and
   Water Pollution.  Report submitted  to U.S. EPA.

 Hernberg S, Nikkanen J. (1970)  Enzyme  inhibition by lead under
   normal urban conditions. Lancet; 1:  63-4.

 Herrera CE, Ferguson JF, Benjamin MM.  (1982)  Evaluating the potential
   for  contaminating drinking water from  the corrosion of tin-antimony
   solder. JAWWA; July: p.  368-675.

 Herrera CE, Kirmeyer GJ, Hoyt BP. (1981, 1982, 1983)   Seattle
  distribution system corrosion control  study. Volumes  1, 2, 3.
  Seattle Water  Department.  Prepared by EPA Municipal Environ-
  mental Research Laboratory; ORD; Cincinnati, Ohio.

Hewitt D, Neri_LC.   (1980)  Development of the  'water story1:  Some
  recent Canadian studies.  Journal of Environmental  Pathology
  and Toxicology; 4 (2 & 3): 51-63.

Hilton PJ (1986). Cellular sodium transport in essential hyper-
  tension.   New England Journal of Medicine;  314:  222-229.

-------
                                -12-
Holtzman D, Shen Hsu J. (1976) Early effects of inorganic lead on
  immature rat brain mitochondrial respiration. Pediatric Res;
  10: 70-5.

Holtzman D, Shen Hsu J, Desautel M. (1981) Absence of effects of
  lead feedings and growth-retardation on mitochondriae and microsomal
  cytochromes in the developing brain. Toxicol Appl Pharmacol;
  58: 48-56.

Hoppenbrouwers T, et al. (1981) Seasonal relationships of sudden
  infant death syndrome and environmental pollutants. American
  Journal of Epidemiology; 113(6).

Horvath SM, Folinsbee LJ. (1979) Effects of pollutants on cardio-
  pulmonary function. Report to U.S. EPA.

Hoyt BP, Kirmeyer GJ, Courchene JE. (1979) Evaluating home plumbing
  corrosion problems.  JAWWA, December; p. 720-725.

Hudson HE Jr, Gilcreas FW. (1976) Health and economic aspects of
  water hardness and corrosiveness. JAWWA; 68: 201-204.

Hudson PJ.  (1966) Fitting segmented curves whose joint points have
  to be estimated. Journal of the American Statistical Association;
  61: 873-80.

Huseman CA, Hassing JM, Sibilia MG. (1986) Endogenous dopaminergic
  dysfunction: A novel form of human growth hormone deficiency and
  short stature.  J. Clin. Endocr. Metab. 62:  484-490.

Hypertension Detection and Follow-up Program Cooperative Group.^
  (1982) The effect of treatment on mortality  in mild hypertension.
  New England Journal of Medicine; 307:  976-80.

lannacone A, Carmignani M, Boscolo P.  (1981) Cardiovascular  reactivity
  in the rat following chronic exposure  to cadmium and lead. Ann
  1st Super Sanita; 17:  655-60.

ICF. (1984) A survey of the literature regarding the relationship
  between measures of  IQ and  income. Prepared  for U.S. EPA,  Office
  of Policy Analysis.

Innes WB.  (1981) Effect of nitrogen oxide emissions on ozone in
  metropolitan  regions. Environmental  Science  and Technology;  15:
  933.

Internal Corrosion of Water Distribution Systems.  (1985) Report of
  the AWWA  Research Foundation  and the DVGW -  .Forschungstelle.

-------
                                 -13-
J.M.  Montgomery  Consulting  Engineers.  (1982  and  1983)  Internal
   Corrosion Mitigation  Study,  Final  Report and Addendum.   Prepared
   for Portland,  Oregon  Water Bureau.

Jackson PJ, Sheiham  I.  (1980)  Calculation of lead  solubility  in
   water.  Water  Research Centre, Technical Report  TR-152.

Jacobson J. (1986) The  costs and benefits of tightening the MCL
   for lead, a  case study of Boston,  Mass. Masters  Thesis;
   Kennedy School of  Government? Harvard University.

Janney A. (1982) The relationship between gasoline lead emissions
   and blood poisoning in Americans.  Prepared for U-.S.  EPA, Office
   of  Policy Analysis.

Johnson NE, Tenuta K. (1979) Diets and lead  blood  levels of children
   who practice pica. Environ Res; 18: 369-376.

Journal of Pediatrics (Editorial). (1977) New approaches to screening
   for iron deficiency;  90:  678.

Kakalik JS, et al. (1981) The  Cost of Special Education. Rand
   Corporation Report N-1791-ED.

Kammholz LP, Thatcher LG, Blodgett FM, Good  TA.  (1972) Rapid proto-
   porphyrin quantitation for detection of lead poisoning. Pediatrics;
Karalekas PC, Craun GF, Hammonds AF, Ryan CR, Worth DJ.  (1975) Lead
  and other trace metals in drinking water in the Boston metropolitan
  area.  Proceedings of the 1975 AWWA Annual Conference; Minneapolis,
  MN.                                                          v     '

Karalekas PC, Ryan CR, Larson CD, Taylor FB. (1978) Alternative
  methods for controlling the corrosion of lead pipe.  Journal of
  the New England Water Works Association; June.

Karalekas PC, Ryan CR, Taylor FB. (1982) Control of lead pipe
  corrosion in the Boston metropolitan area. Proceedings of the
  1982 AWWA Annual Conference; Miami Beach, Florida.

Karalekas PC, Ryan CR, Taylor FB. (1983) Control of lead, copper,
  and iron pipe corrosion in Boston. JAWWA; February.

Karalekas PC. (1984) Impact of lead piping and fittings on drinking
  water quality. Proceedings of a Seminar on Plumbing Materials
  and Drinking Water Quality. Sponsored by US EPA; Cincinnati,
  Ohio; May.

Keller CA and Doherty RA.  (1980a) Bone lead mobilization in lac-
  tating mice and lead transfer to sucking offspring. Toxicol. Appl.
  Pharmacol. 55: 220-228.

Keller CA and Doherty RA.  (1980b) Lead and calcium distributions in
  blood, plasma, and milk of the lactating mouse. J.Lab. Clin. Med.
  95: 81-89.

-------
                                -14-
Kennedy Engineers. (1973) Seattle Corrosion Study (initial); Tacoma,
  Washington.

Kennedy Engineers. (1978) Internal corrosion study, summary report.
  Conducted for the city of Seattle, Washington; February.

Khera AK, Wibberley DG, Edwards KW, Waldron HA. (1980) Cadmium and
  lead levels in blood and urine in a series of cardiovascular and
  normotensive patients.  Intern J Environ Studies; 14: 309-312.

Kirkby H, Gyntelberg F.  (1985) Blood pressure and other cardio-
  vascular risk factors of long-term exposure to lead.  Scand J
  Work Envir Health; 11: 15-19.

Kirmeyer GJ, Logsdon GS. (1983) Principles of internal corrosion
  and corrosion monitoring. JAWWA; February; p. 78-83.

Klein JP, et al.  (1980) Hemoglobin affinity for oxygen during
  short-term exhaustive  exercise. Journal of Applied Physiology; 48.
Kleinbaum DG, Morgenstern H, Keyser LL.
  Research.
(1982)  Epidemiologic
Kobayashi J.  (1957) On geographical  relationship between the chemical
  nature of  river water  and  death-rate  from  apoplexy. Berichte des
  Ohara Instituts fur landwirtschaftliche, Biologie;  11: 12-21.

Kopp  SJ, Baker  JC, D'Agrosa  LS;  Hawley  PL.  (1978)  Simultaneous
  recording  of  his bundle  electrogram,  electrocardiogram,  and sys-
  tolic tension from  intact  modified Langendorff rat  heart prepara-
  tions. I:  effects of perfusion time,  cadmium, and lead.  Toxicol.
  Appl. Pharmacol. 46: 475-487.

Kopp  SJ, Glonek T, Erlanger  M,  Perry EF,  Perry HM  Jr, Barany M.
   (1980) Cadmium and  lead  effects on myocardial function and
  metabolism.   J Environ Pathol Toxicol;  4:  205-27.

Kromhout D,  Couland CL.  (1984)  Trace metals  and CHD risk  indicators
   in  152 elderly men  (the  Zutphen Study).  Eur Heart J;  5  (Abstr
   suppl  1):   101.

Kromhout D,  Wibowo AA, Berber RF, Dalderup LM, Heerdink H, de  Lezenne
   Coulander C,  Zielhuis  RL.  (1985) Trace metals  and coronary  heart
   disease  risk  indicators  in 152 elderly men (the  Zutphen  study).
   American Journal  of Epidemiology;  122: 378-385.

Kuch  A, Wagner  I.  (1983) A mass transfer model to  describe lead
   concentrations in  drinking water.  Water Research;  17  (10):
   1303-1307.

 Lamola A-A,  Joselow M,  Yamane T.  (1975a) Zinc protoporphyrin  (ZPP):
   a simple, sensitive,  fluorometric screening test for lead poison-
   ing. Clin Chem (Winston Salem, NC); 21: 93-7.

-------
                                  -15-
 Lamola A-A,  Piomelli S,  Poh-Fitzpatrick MB, Yamane T, Harber LC.
   (1975b) Erythropoietic protoporphyria and lead intoxication: the
   molecular  basis for difference in cutaneous photosensitivity:
   II.  different binding  of erythrocyte protoporphyrin to hemo-
   globin. J  Clin Invest; 56:  1528-5.

 Landis JR and Flegal KM. (1986) Randomization model tests for the
   regression of blood pressure on blood lead using NHANES II data.
   American Journal of Epidemiology.

 Landrigan PJ,  Baker EL,  Peldmari RG, Cox DH, Eden KV,  Orenstein WA,
   Mather JA,  Yankel AJ,  von Lindern IH. (1976) Increased lead
   absorption with anemia and  slower nerve conduction in children
   near a lead smelter. Journal of Pediatrics;  89: 904-10.
 Larson  TE,  King RM.
   JAWWA;  January.
(1954)  Corrosion by water at low flow velocity,
 Larson  TE.  (1955)  Report  on loss  in carrrying capacity of water
   mains;  JAWWA.

 Larson  TE.  (1966)  Deterioration of  water quality  in distribution
   systems.  JAWWA;  58  (10):  1307-1316.

 Larson  TE,  McGurk  FF.  (1973) Complexes  affecting  the solubility of
   calcium carbonate in water. Final report. University of Illinois
   Water Resources  Center.

 Larson  TE.  (1976)  Corrosion by  domestic waters. Illinois  State
   Water Survey, Urbana 1975 (also published in W&SE,  p. R-176
   to R-183).

 Larson  TE,  Sollo FW, McGurk FF. (1976)  Complexes  affecting the
   solubility of calcium carbonate in water -  Phase  II.  Final Report
   University of Illinois Water  Resources Center.

 Lassovszky  P, Hanson H.   (1983) Regulatory and operational aspects
   of controlling corrosion  by-products  from water supply  distribu-
   tion  systems.  AWWA  Conference on Water Quality and Treatment:
   Advances  in Laboratory Technology; Pennsylvania.

 Lassovszky  P. (1984) Effect on water quality  from lead  and nonlead
   solders in piping. Heating/Piping/Air Conditioning;  October;
   p. 51—58.

 Lauwerys R, Buchet JP, Roels H,  Hubermont G.  (1978)  Placental
   transfer  of lead, mercury, cadmium, and carbon  monoxide  in women.
   I. Comparison of the frequency distributions of the biological
   indices in maternal and umbilical cord blood. Environmental
   Research; 15: 278-89.

Lave L,  Seskin E.   (1977) Air Pollution  and Human Health. Johns
  Hopkins University Press; Baltimore.	~

-------
                                -16-
Laxen DPH, Harrison RM. (1977) The highway as a source of water
  pollution. Water Research; 11:__ 1-11.

Lead Industries Association. (1982) Solders and Soldering:  A
  Primer.  L.I.A., Inc; New York.

Leighton J, Shehadi A, Wolcott R.  (1983) Aggregate benefits of air >
  pollution control. Prepared for U.S. EPA, Office of Policy Analysis,
  by Public Interest Economics Foundation; Washington, DC; June.

Levy RI.  (1984) The decline in coronary heart disease mortality:
  Status and perspective on the role of cholesterol. American
  Journal of Cardiology; August 27; 54  (4).

Lewis BW, Collin RJ, Wilson HS. (1955) Seasonal incidence of lead
  poisoning in children in St. Louis. Southern Medical Journal;
  48: 298-301.

Lilienfeld AM, Lilienfeld DE.  (1980) Foundations of Epidemiology.
  Oxford  U Press, New  York.

Lincoln RH. (1984) Written statement before the Senate Committee on
  Environmental and Public Works  in Opposition to Senate  Bill  2609.

Lin-Fu JS.  (1973) Vulnerability of children to lead exposure and
  toxicity: parts one  and two. New England Journal of Medicine;
  289: 1229-33, 1289-93.

Lin-Fu JS.  (1982) The  evolution of childhood  lead poisoning as a
  public  health problem.  In:  Chisholm  JJ  and O'Hara DM  (eds).  Lead
  Absorption  in Children. Urban and Schwarzenberg, Inc.,  Baltimore;
  p.  1-10.

Litman DA,  Corriea MA. (1983)  L-tryptophan:   a common denominator
  of  biochemial and neurological  events of acute hepatic  porphyrias?
  Science;  222: 1031-3.

Lorimer  G.  (1886) Saturnine  gout,  and its  distinguishing  marks.
  British Medical Journal.

Lovell  J, Isaac R,  Singer R.  (1978) Control  of  lead  and  copper in
  private water  supplies. Carroll County Health Department;  Carroll
  County, Maryland.

Levering TG (ed).  (1976)  Lead in the  environment.  US  Geological
  Survey paper #957;  USGPO.

Lyon  TDB, Lenihan JMA. (1977) Corrosion in solder-jointed copper
   tubes resulting in  lead  contamination of drinking  water.  British
  Corrosion Journal;  12(1):  41.

-------
                                 -17-
 Maessen 0,  Freedman B,  McCurdy R.  (1985)  Metal mobilization in
   home well water systems in Nova  Scotia.   JAWWA;  June;  p.  73-80.

 Mahaffey KR,,Rader J.  (1980) Metabolic interactions:  lead,
   calcium and  iron.  Annals of the  NY Academy of Sciences;  355:
   •&o5— 297 .
 Mahaffey  KR.( 1981)  Nutritional  factors  in lead poisoning.  Nutr Rev;
   •3 J. *  ODo"~
 Mahaffey  KR, Annest  JL,  Roberts  J,  Murphy  MS.  (1982a)  National
   estimation of  blood  lead  levels:  United  States  (1976-1980). New
   England Journal  of Medicine; 307:  573-9.

 Mahaffey  KR, Rosen JF, Chesney RW,  Peeler  JT,  Smith  CM,  DeLuca  HF.
   (1982b)  Association  between age,  blood lead  concentrations and
   serum 1,25-dihydroxycholecalciferol  levels in children. American
   Journal of Clinical  Nutrition;  35: 1327-31.

 Mahaffey  KR, Annest  JL.  (1986) Association of  erythrocyte proto-
   porphynn with blood lead level and  iron status  in the NHANES II,
   1976-1980. Environmental Research; 41: 327-338.

 Mahaffey  KR, Gartside  PS, Glueck CJ. (1986) Blood  lead levels and
   dietary calcium  intake in 1-11 year  old children:  NHANES II,
   1976-1980.. Pediatrics; 78(2): 257-262.

 Manton wi. (1977)  Sources of lead in blood: identification by
   stable  isotopes. Archives of Environmental Health; 32: 149-59.

 Matlack W F. (1980) Statistics for Public Policy and Management.
   Duxbury  Press; Massachusetts.             ~ — - -

McBride WG, Black  BP, English BJ. (1982) Blood lead levels and
   behavior of 400  preschool children. Med Journal Aust; 2: 26-9.

McCabe LJ, Symons  JM, Lee RD, Robeck GG. (1970) Survey of community
  water supply systems.  JAWWA; 62(11): 680-687.

McCauley PT, Bull RJ. (1978) Lead-induced delays in synaptogenesis
   in the rat cerebral cortex. Fed Proc Fed Am Soc Exp Bio; 37:  740.

-------
                                -18-
McGee Dr Gordon T. (1976) The results of the Framingham study
  applied to four other U.S-based epidemiologic studies of
  coronary heart disease.  The Framingham Study; Section 31.
  DHEW Pub No. (NIH) 76-1083.  National Institutes of Health;
  U.S. Government Printing Office, Washington, B.C.

McMichael AJ, Vimpani GV, Robertson EF, Baghurst PA, Clark PD. (1986)
  The Port Porie Cohort Study:  Maternal blood lead and pregnancy
  outcome. J Epidemiol Commun Health; 40: 18-25.

Mellins RB, Jenkins CD.  (1955) Epidemiological and psychological
  study of lead poisoning in children. Journal of the American Medical
  Association; 158: 15-20.

Mentzer WC.  (1973) Differentiation of iron deficiency from thalessemia
  trait. Lancet;  1: 882.

Meranger JC, Subramanian KS, Chalifoux C.  (1979) A national  survey
  for cadmium, chromium, copper,  lead, zinc,  calcium and magne-
  sium  in Canadian drinking water supplies.   Environmental  Science
  and Technology; 13(6): 707-711.

Meredith PA, Moore MR, Campbell  BC,  Thompson  GG, Goldberg A.  (1978)
  Delta-aminolevulinic acid metabolism  in  normal and lead-exposed
  humans.  Toxicology; 9:  1-9.

Midwest Research  Institute.  (1979) Occurrence and  impacts of
  aggressive water  systems.  MRI  publication.

Milar CR,  Schroeder  SR,. Mushak  P, Dolcourt J, Grant  LD.  (1980)
  Contributions  of  the caregiving environment to  increased  lead
  burden  of  children.  American  Journal  Mental Deficiency; 84:
  339-44.

Milar CR,  Schroeder SR,  Mushak  P, Boone L. (1981)  Failure to find
  hyperactivity in preschool children with moderately  elevated lead
   burden.  Journal Pediatric Psychology;  6: 85-95.

 Miller RG, Greathouse D, Bull RJ, Doerger JU. (1985)  Absorption of
   lead from drinking water with varying mineral content.   In:
   Calabrese E et al., Inorganics in Drinking Water and Cardiovascular
   Disease; Princeton Scientific Press; New Jersey.

 Millette JR, Hammonds AF, Pansing MF, Hanson EC, Clark PJ.
   (1980)  Aggressive water:  assessing the extent of the problem.
   JAWWA;  72 (5):  262-66.

-------
                                 -19-
 Minnesota Department of Health.  (1985)  Preliminary Study of
   Community Water Systems.   Conducted by the Water Supply and
   Engineering Section,  Minnesota Department of Health.

 MITRE  Corporation.  (1979) The  environmental lead problem:   An
   assessment of lead in drinking water from a multi-media prospec-
   tive.   Prepared for U.S.  EPA,  Office  of Drinking Water;  May.

 Moore  MR.  (1973)  Plumbosolvency  of  waters.  Nature; 243:  222-223.

 Moore  MR,  Meredith  PA.  (1976)  The association of delta aminolevulinic
   acid with the neurological and behavioral effects of lead exposure.
   In:  Hemphill  DD ed, Trace  Substances  in Environmental  Health - X.
   University of Missouri; Columbia, MO.	

 Moore  MR,  Goldberg  A, Pocock SJ,  Meredith A,  Stewart  IM,
   Macanespie H,  Lees  R,  Low  A.   (1982)  Some studies of maternal
   and  infant lead exposure  in  Glascow.  Scottish  Medical  Journal;
   £i*  113—122.

 Moore  MR.  Uptake  of  lead from  water.  (1985)  In:   Calabrese  E  et
   al.  (ed),  Inorganics  in Drinking Water  and  Cardiovascular Disease.
   Princeton  Scientific  Press;  New Jersey.     ~	

 Mooty  J, Ferand  DP Jr,  Harris  P.  (1975) Relationship  of  diet  to
   lead poisoning  in children.  Pediatrics; 55:  636-639.

 Morbidity  and Mortality Weekly Reports, various  issues,  1976-1981,
   U.S. Public Health Service.

Morbidity  and Mortality Weekly Reports:  Reports  of the Lead
   Poisoning Prevention Screening  Program 1973-1981.

Morgan JM.  (1976) Hyperkalemia and acidosis in lead neuropathy.
  South Med J; 69(7):  881-3.

Moreau T, Orssaud G, Juguet B,  Busquet G. (1982) Plombemie et
  pression arterielle: premiers resultats d'une enquete transvers-
  able de 431 sujets de sexe masculin.  [Blood lead levels and
  arterial pressure: initial results of a cross sectional study of
  431 male subjects.] [Letter]  Rev Epidemol Sante Fpulique; 30:
  •3-7 O~" / •

-------
                                -20-
Moriarity M. (1978) Role of calcium in the regulation of adeno-
  hypohysial hormone release. Life Sciences; 23: 184-185.

Mouw DR, Vander AJ, Cox Jf Fleischer N. (1978) Acute^effects^of
  lead on renal electrolyte excretion and plasma renin activity.
  Toxicol Appl Pharmacol; 46-: 435-447.

Mruk SA. (1984) Plastic piping and piping materials.  Presented
  at the Plumbing Materials and Drinking Water Quality Seminar;
  sponsored by EPA; Cincinnati, Ohio; May.

Mullen ED, Hitter JA. (1980) Monitoring and controlling corrosion
  by potable water. JAWWA; May; p. 286-291.

Multiple Risk Factor Intervention Trial:  Risk  factor changes  and
  mortality results. Multiple Risk Factor Intervention Trial   _
  Research Group.  (1982) Journal of the American Medical Association;
  248: 1465-77.

Murrell NE.  (1984) Summary of impact  of metallic solders on water  _
  quality.  Proceedings  of Seminar on Plumbing  Materials and Drinking
  Water Quality. Sponsored by US-EPA; Cincinnati, Ohio; May.

Murrell NE.  (1985) Impact of metallic solders on water quality.   _
  Presented  at the Specialty Conference on  Environmental Engineering;
  American  Society of Corrosion Engineers;  Boston.

Murrell NE,  Holzmacher,  McClendon.  (1982) Lead  in drinking water  due
  to  lead-tin  solder  joints  utilized  in interior residential and
  other plumbing.  H2M Corporation; New York.

Nassau  County  Department of  Health.  (1985)  Report of  Investigation
  of  Drinking  Water  Contamination  by  Lead/Tin Solder  in  Nassau County,
  New York,  New  York; August.

National Academy of  Sciences.  (1972)  Lead:  airborne lead in perspec-
  tive. National Academy of  Sciences; Washington, DC.  (Biologic
  Effects  of Atmospheric Pollutants  series.)

National Academy of  Sciences.  (1977-1982)  Drinking  Water and Health.
  Safe  Drinking  Water Committee.  (4-volume  study) National  Academy
  of  Sciences; Washington,  D.C.

National  Center  for  Health Statistics.  National Hospital Discharge
  Survey,  various  issues.

-------
                                -21-
National Center  for Health  Statistics.   (1981)  Plan  and Opera-
   tion of the Second National Health  and Nutrition Examination
   Survey (1976-1980).  National Center  for Health Statistics.  (Vital
   and Health Statistics Series 1, No. 15).

Needleman EL, Gunnoe C, Leviton A, Reed R, Peresie H, Maher C,
   Barret P. (1979) Deficits  in psychological and classroom per-
   formance of children with  elevated  dentine lead levels. New
   England Journal of Medicine; 300: 689-95.

Needleman HL. (1981) The neurobehavioral consequences of low lead
   exposure in childhood. Neurobehav Toxicol Teratol; 4: 729-732.

Needleman HL. (1984) Comments on chapter 12 and appendix 12C, Air
   Quality Criteria for Lead  (external review draft #1). Available
   for inspection at: U.S. Environmental Protection Agency, Central
   Docket Section, Washington, DC; docket no. ECAO-CD-81-211
   A.E.G.1.20.

Needleman HL, Bellinger D.  (1984) The developmental consequences
   of childhood exposure to lead: recent studies and methodological
   issues.  In:  Lahey BB, Kazdin AE, eds. Advances in Clinical
   Child Psychology; v. 7; Plenum Press; New York, NY; p. 195-220.

Needleman HL, Landrigan PJ.  (1981) The health effects of low level
   exposure to lead. Ann Rev Public Health; 2: 277-298.

Needleman HL, Leviton A, Bellinger D. (1982) Lead-associated
   intellectual deficit [letter]. New England Journal of Medicine;
   306: 367.

Needleman HL, Geiger SK, Frank R. (1985) Lead and IQ scores: a
   reanalysis [letter]. Science;  227: 701-704.

Needleman HL, Rabinowitz M, Leviton A, Linn S,  Schoenbaum S. (1984)
  The relationship between prenatal exposure to lead and congenital
  anomalies.  Journal of the American Medical Association:  251-
  2956-9.

Neff CH.  (1984)  Impact of copper, galvanized pipe,  and fittings on
  water quality.  Presented at the Plumbing Materials and  Drinking
  Water Quality Seminar; sponsored by EPA;  Cincinnati, Ohio.

-------
                                -22-
Neff CH, Schock MR. (1985) Corrosion product — corrosion rate --
  water quality investigation in building systems.  Prepared for
  uts? EPA, Drinking Water Research Division; Cincinnati, Ohio.

Neff CH, Schock MR, Marden JI.  (1987) Relationship Between water
  duality and corrosion of plumbing materials in buildings.
  Prepared for Ss-EPA Drinking Water Research Division; Cincinnati,
  Ohio  (in press).

New approaches to  screening for iron deficiency. Editorial.
  Journal of Pediatrics;  90:  678.

Nielsen K.  (1975)  Contamination of drinking water by cadmium and
  lead  from fittings. Danish  Building Research  Institute.

Nielsen K   (1976)  Dissolution of materials  from service  pipes  and
  houle installations and its sanitary  aspects.  International  Water
  Supply Association. Amsterdam Conference.

Nielsen K.  (1984)  Corrosion of  soldered and brazed  joints  in tap
  water. British Corrosion Journal;  19(2):  57-bJ.

Nordstrom  S,  Beckman  L,  Nordenson  I.  (1978a)  Occupational  and
   environmental  risks in and  around  a  smelter in northern  Sweden:
   I.  variations  in birth weight.   Hereditas;  88: 43-46.

Nordstrom  S,  Beckman  L,  Nordenson I.  (1978b)  Occupational  and
   environmental  risks in and  around  a  smeIter ^V^S. 51-54
   III.  frequencies of spontaneous abortion. Hereditas; 88: 51-54.

Nordstrom S,  Beckman L,  Nordenson I.  (1979a)  Occupational  and
   environmental risks in and around a smelter in northern Sweden:
   ^spontaneous abortion among female employees and decreased
   birth weight in their offspring. Hereditas; 90: 291-296.

 Nordstrom S,  Beckman L,  Nordenson I. (1979b) Occupational and
   environmental risks in and around a amelter in northern Sweden:
   VI. congenital malformations. Hereditas; 90;  297-302.

 Nye LJJ.  (1929) An investigation of the  extraordinary incidence of
   chronic nephritis in young people in Queensland. Med J Aust,
   2: 145-159.

-------
                                 -23-
 O'Brien JE.  (1976)  Lead in Boston:  its cause and prevention.  Journal
   of  the New England Water Works  Association;  90(2):  173-180.

 Odenbro A, Greenberg N,  Vroegh  K, Bederka J, Kihlstrom JE.  (1983)
   Functional disturbances  in  lead-exposed children. Ambio;  12:
   40-4.

 Oliphant RJ.  (1982)  Lead contamination of potable water arising
   from  soldered  joints.  IWSA  Congress?  Zurich.

 Oliphant RJ.  (1983)  Lead contamination of potable water arising  from
   soldered joints.   Water  Research  Centre Report #125E.   England.

 Otto  DA,  Benignus VA, Muller  KE,  Barton CN.  (1981) Effects  of age
   and body lead  burden  on  CNS function in young  children. I:  slow
   cortical potentials.  Electroencephalog  Clin Neurophysiol; 52:
   229—39.

 Otto  DA  et al. (1982) Effects of  low to moderate lead  exposure on
   slow  cortical  potentials  in young children:  two-year follow-up
   study.  Neurobehav Toxicol  Teratol;  4:  733-7.

 Otto  D, Robinson G,  Baumann S, Schroeder  S,  Kleinbaum  D, Barton  C,
   Mushak  P, Boone L.  (1984) Five-year  follow-up  study  of children
   with  low-to-moderate  lead absorption:   electrophysiological
   evaluation.  Presented at the Second  International Conference  on
   Prospective Lead Studies; Cincinnati, OH. Available  for inspection
   at: U.S. Environmental Protection Agency, Environmental Criteria
   Assessment Office, Research Triangle  Park, NC.

 Paglia DE, Valentine WN, Dahlgren JG.  (1975) Effects of low level
   lead exposure  on pyrimidine 5'  nucleotidase and other erythrocyte
   enzymes:  possible role of pyrimidine 5' nucleotidase in the
   pathogenesis of lead induced anemia.  Journal of Clinical Inves-
   tigation; 56:  1164-9.

Patterson JW. (1978) Corrosion inhibitors and coatings. Proceedings
   of the AWWA annual meeting;  June.

Patterson JW. (1981) Corrosion in water distribution systems.
  Prepared for U.S.  EPA, Office of Drinking Water; March.

Patterson JW, O'Brien JE. (1979) Control of lead corrosion.  JAWWA;
  71(5): 264-271.

-------
                                -24-
Paul C. (1860) Etude sur 1'intoxication lente par les preparations
  de plomb, de son influence sur le produit de la conception LStudy
  of the effect of slow lead intoxication on the product of concep-
  tion].  Arch Gen Med; 15:  513-533.

Perino J, Ernhart CB.  (1974) The relation of subclinical lead level
  to cognitive and sensorimotor impairment in black preschoolers.
  Journal of Learning Disabilities; 7: 616-620.

Perkin - Elmer. (1977) Analytical Methods for Atomic Absorption
  Spectrophotometry Using the HGA Graphic Furnace. Norwalk,
  Connecticut.

Perlstein MA, Attala R. (1966) Neurologic sequelae of plumbism in
  children.  Clinic Pediatric  (Philadelphia); 5: 292-8.

Perry HM Jr, Erlanger  MW. (1978) Pressor effects of chronically
  feeding cadmium and  lead together.  In Hemphill DD  (ed). Trace   <
  Substances in Environmental Health-XII;  Proceedings of University
  of Missouri's 12th annual conference on trace substances in
  environmental health; June; University of Missouri-Columbia;
  Columbia, MO: p. 268-75.

Perry HM.  (1984) Environmental heavy  metals and human cardiovascular
  disease.  In Bell and Doege  (eds), Drinking Water and Human Health.
  American Medical Association.

Petrusz P,  Weaver CA,  Grant LD,  et al.  (1979)  Lead poisoning and
  reproduction: effects on pituitary  and serum gonadotropins in
  neonatal rats. Environ  Res;  19:  382-391.

Piccinini  F,  Favalli L, Chiari MC.  (1977)  Experimental  investigations
  on the contractions  induced by lead in arterial  smooth muscle.
  Toxicology;  8: 43-51.

Piomelli S, Davidow B, Guinee VF,  Yound P,  Gay G.  (1973) The FEP
   (free erythrocyte porphyrins)  test:  a  screening micromethod for
   lead poisoning.  Pediatrics; 51:  254-9.

 Piomelli S, Seaman C,  Zullow D,  Curran A,  Davidow B.  (1977)  Metabolic
   evidence of lead toxicity in "normal" urban children.  Clinic Res;
   25: 459A.

 Piomelli S, Seaman C,  Zullow D,  Curran A,  Davidow B. (1982)  Threshold
   for lead damage to heme synthesis in urban children.  Proceeding
   of the National Academy of Sciences in May; 79: 3335-9.

-------
                                 -25-
 Piomelli Sf Rosen JF, Chisolm JJ, Graef JW. (1984) Management of
   childhood lead poisoning.  Pediatrics; 4: 105.

 Pirkle JL, Annest JL. (1984) Blood lead levels 1976-1980 - Reply
   (letter).  New England Journal of Medicine;  310(17):  1125-6.

 Pirkle J.L, Schwartz J,  Landis JR, Harlan WR.  (1985)  The relationship
   between ^ blood lead levels  and blood pressure and its  cardiovas-
              imPlications' American Journal of Epidemiology;  121(2):
 Pocock SJ.  (1980)  Factors  influencing  household  water lead:   a British
   national  survey.  Archives  of  Environmental  Health;  35(1):  45-51.

 Pocock SJ,  Shaper  AG, Walker M, Wale CJ,  Clayton Bf Delves T,
   Lacey RF,  Packam RF,  Powell P.  (1983) Effects  of  tap water lead,
   water hardness,  alcohol, and  cigarettes on  blood  lead concentrations.
   J  Epidemiol  Comm Health; 37:  1-7.

 Pocock SJ,  Shaper  AG, Ashby  D,  Delves  T,  Whitehead  TP.  (1984)
   Blood lead concentration,  blood pressure, and  renal function.
   British Medical  Journal; 289s 872-874.

 Pocock SJ,  Shaper AG, Ashby  D,  Delves  T.  (1985)  Blood lead and blood
   pressure  in  middle-aged men.  In: Lekkas  TD  (ed),  International
   Conference on Heavy Metals in the Environment.  September;  Athens,
   Greece .

 Pocock  SJ, Ashby D.  (1986) Environmental  lead and children's intelli-
   gence: a  review of recent  epidemiological studies.  Statistician.

 The  Pooling  Project Research  Group. (1978) Relationship of blood
   pressure,  serum cholesterol, smoking habit, relative weight  and
   ECG  abnormalities to  incidence of major  coronary events:   Final
   report of  the Pooling Project. J Chron Dis; 31: 201-306.

 Port CD. (1977) A comparative study of experimental and spontaneous
   emphysema. J Toxicol Environ Health;  2:   589-604.

 Pounds JG, Wright R, Morrison D, Casciano DA.  (1982a)  Effect of
   lead on calcium homeostasis in the isolated rat hepatocyte.
  Toxicol Appl Pharmacol; 63: 389-401.

 Pounds JG, Wright R, Kodell RL.  (1982b) Cellular metabolism of lead:
                                         hepatocyte. Toxicol Appl
Pounds JG, Mittelstaedt RA. (1983) Mobilization-of cellular Ca-45
  fnj lead-210:  effe°t of physiologic stimuli. Science; 220:
  308—3 10 .

-------
                                -26-
Pounds JG. (1984) Effect of lead intoxication on calcium homeostasis
  and calcium-mediated cell function:  a review.  Neurotoxicology;
  5: 295-332.

Pounds JG, Rosen JF. (1986) Cellular metabolism of lead:  a
  kinetic analysis in cultured osteoclastic bone cells.  Toxi-
  cology and Applied Pharmacology; 83: 531-545.

Prentice RC, Kopp SJ. (1985) Cardiotoxicity of lead at various per-
  fusate calcium concentrations:  functional and metabolic responses
  of the perfused rat heart.  Toxicol Appl Pharmacol? 81: 491-501.

Provenzano G. (1980) The social costs of excessive lead-exposure
  during childhood. In:  Needleman (ed); Low Level Lead Exposure;
  The Clinical Implications of Current Research. Raven Press, New
  York.	

Provvedini DM, Tsoukas CD, Deftos LJ, Manolagas SC.  (1983) 1,25-
  dihydroxy-vitamin D3 receptors in human leukocytes. Science;
  221: 1181-2.

Public Use Data Tape Documentation, Hematology and Biochemistry.
  (1976-1980).  Second National Health and Nutrition Examination
  Survey. Catalog number 5411, U.S. Public Health Service, National
  Center for Health Statistics.

Quarterman J, Morrison J, Humphries W.  (1978) The influence of high
  dietary calcium and phosphate on lead uptake and release.  Environ-
  mental Research; 17: 60-67.

Rabinowitz MB, Wetherill GW, Kopple JD.  (1976) Kinetic analysis of
  lead metabolism in human health. Journal of Clinical Investigation;
  58: 260-70.

Rabinowitz MB, Wetherill GW, Kopple JD.  (1977) Magnitude  of  lead
  intake  from respiration by normal man. Journal of  Laboratory and
  Clinical Medicine; 90: 238-248.

Rabinowitz MB, Kopple JD, Wetherill GW.  (1980)  Effect  of  food intake
  and fasting on gastrointestinal  lead  absorption in humans.  Am J
  Clin Nutr; 33: 1784-1788.

Rabinowitz MB, Needleman H.  (1982) Temporal  trends in  the lead
  concentrations of  umbilical  cord blood.  Science; 216:  1429-1431.

Rabinowitz MB, Needleman H.  (1983) Petrol  lead  sales and umbilical
  cord blood lead  levels in Boston,  Massachusetts; Lancet.

Rabinowitz MB, Leviton A, Needleman  H.  (1984)  Variability of blood
  lead concentrations  during  infancy. Archives  of Environmental
  Health;  39:  74-77.

Ramirez-Cervantes  B, Embree JW, Hine CH, Nelson KM,  Varner MO,
  Putnam RD.  (1978)  Health  assessment of employees with different
  body burdens of  lead. Journal Occupational Medicine;  20: 610-7.

-------
                                 -27-
 Randall  A,  et al.  (1974)  Bidding games for valuation of aesthetic
   environmental  improvements.  J Environ Econ Manag;  1:  132-49.

 Rasmussen H,  Waisman  DM.  (1983)  Modulation of cell function in  the
   calcium messenger system.  Rev Physiol Biochemical  Pharmacol;  95:
   J. J. J.~4o •

 Report of Commissioners,  Appointed  by  Authority  of the  City Council
   to Examine  the Sources  from  Which a  Supply of  Pure Water May  Be
   Obtained  for the City of Boston.  (1845)  JH Eastburn,  City Printer,
   Boston.

 Revis NW, Schmoyer RL, Bull  R.  (1982)  The  relationship  of  minerals
   commonly  found in drinking water  to  atherosclerosis and  hyper-
   tension in  pigeons; JAWWA; December;  p.  656-659.

 Richards WN,  Moore MR. (1982)  Plumbosolvency in  Scotland - the
   problem,  remedial action taken  and health  benefits observed.
   JAWWA; May;  p. 901-918.

 Richards WN,  Moore MR. (1984)  Lead  hazard  controlled in Scotish water
   systems.  JAWWA; August? p. 60-67.

 Richet G, Albahary C, Morel-Maroqer L,  Guillaume P,  Galle  P.  (1966)
   Les alterations renales dans  23 cas  de saturnisme  professionnel.
   [Renal changes in 23 cases of occupational  lead  poisoning]  Bull
   Memorial  Society Medical Hop Paris;  117: 441-66.

 Robins JM,  Cullen MR, Connors BB, et al. (1983) Depressed  thyroid
   indexes .associated with occupational  exposure to inorganic  lead.
   Arch Int  Med; 143: 220-224.

Roels H, Buchet JP, Lauwerys R, Hubermont G,  Braux P, Claeys-
  Thoreau F,  LaFontaine A, Van Overschelde J.  (1976)  Impact of air
  pollution by lead on the heme biosynthetic  pathway  in school aqe
   children.  Arch Environ Health; 31: 310-6.

Rohn RD, Shelton JE, Hill JR.  (1982) Somatomedin activity  before and
   after chelation therapy in lead-intoxicated children.  Arch Envir
  Health; 37:  369-373.

Rom WN.  (1976) Effects of lead on the female and reproduction: a
  review.  Mt. Sinai Journal of Medicine; 43: 542-552.

-------
                                -28-
Rosen JF. (1983) The metabolism of lead in isolated bone cell
  populations: interactions between lead and calcium. Toxicol Appl
  Pharmacol; 71: 101-112.

Rosen JF, Chesney RW, Hamstra A, De Luca HF, Mahaffey KR. (1980a)
  Reduction in If25-dihydroxyvitamin D in children with increased
  lead absorption. New England Journal of Medicine; 302: 1128-31.

Rosen JF, Chesney RW, Hamstra A, DeLuca HF, Mahaffey KR. (1980b)
  Reduction in 1,25-dihydroxyvitamin D in children with increased
  lead absorption.  Brown SS, Davis DS ed. Organ Directed Toxicity
  Chemical Indices and Mechanisms; Pergamon Press, New York, NY.

Rosen JF, Chesney RW. (1983) Circulating calcitriol concentrations
  in health and disease. Journal Pediatr (St. Louis); 103: 1-7.

Routh DK, Mushak P, Boone L. (1979) A new syndrome of elevated
  blood lead and microcephaly. J Pediatr Psychol; 4: 67-76.

Royal Comission on Environmental Pollution.  (1983) Ninth report -
  lead in the environment. Cmnd 8852, Her Majesty's Stationery
  Office? London, England.

Rummo JH (1974) Intellectual and behavioral  effects of lead poison-
  ing in children. Dissertation; University  of North Carolina.
  (Available also on University Microfilms.)

Rummo JH, Routh DK, Rummo NJ, Brown JF.  (1979) Behavioral and
  neurological effects of symptomatic and asymptomatic lead-exposure
  in children.  Archives of Environmental Health; 34(2): 120-4.

Ryder RR.  (1980) The costs of internal corrosion  in water systems.
  JAWWA; May; p. 267-279.

Ryu JE,  Ziegler EE, Nelson SE,  Fomon SJ.  (1983) Dietary  intake  of
  lead and  blood lead concentration in early infancy.  Am J Dis
  Child; 137: 886-891.

Saenger  P,  Markowitz ME, Rosen  JF.  (1984) Depressed  excretion of  6
  hydroxycortisol in lead-toxic children.   J Clin Endocrinol Metab;
  58: 363-367.

Samuels  ER, Meranger JC.  (1984) Preliminary studies  on  the  leaching
  of some metals from kitchen faucets.   Water Research;  18  (1):
  75-80.
 Sandstead  HH,  Orth  DN,  Abe  K,  et  al.  (1970)  Lead  intoxication:
   effect on  pituitary  and adrenal function in man.   r-iin  *««=•
   18:  76.
Clin Res;

-------
                                 -29-
 Sandstead HH,  Stant EG,  Brill B,  et al.  (1969)  Lead intoxication
   and the thyroid.  Arch  Intern Med; 123:  632-635.

 Sartor F,  Van  Beneden P,  Rondia D.  (1981)  Water lead concentrations
   and measurements  of health risk in a soft water  drinking area.
   Presented  at the  Heavy Metals in  the Environment conference,
   Amsterdam; September.

 SAS Users  Guide.  (1982)  Statistical Analysis System,  Inc.  Gary,  NC.

 Sassa S,  Garnick  JL,  Garnick S,  Kappas A,  Levere RD.  (1973)
   Studies  in lead poisoning.  I:  Microanalysis of erythrocyte  proto-
   porphyrin  levels  by spectrofluorometry in the detection  of  chronic
   f??d>,ontoxication in the  subclinical range. Biochem Medical; 8:
   135—48.

 Sauer HI.  (1980)  Geographic patterns in the risk of  dying  and
   associated factors,  US  1968-1972.  DHHS Publication (PHS) 80-1402;
   Vital and Health  Statistics;  GPO  Washington,  DC.

 Schock MR. (1980  and  1981)  Response of lead solubility to  dissolved
   carbonate  in drinking water.  JAWWA;  72 (12):  695,  December  and
   Errata,  73 (3): 36,  March.

 Schock MR, Gardels  MC. (1983)  Plumbosolvency reduction by high pH
   and low  carbonate-solubility relationships. JAWWA;  75  (2):  87-91.

 Schroeder  HA.  (1958)  Degenerative cardiovascular disease in the
   Orient.  Journal  of Chronic  Disease; 8:  312-333.

 Schroeder  SR, Hawk  B, Otto  DA, Mushak  P, Hicks  RE.  (1984/1985)
   Separating the  effects of lead and social  factors on IQ.  in:
   Bornschein and .Rabinowitz  (eds).  The Second  International  Con
   ference on Prospective Studies of Lead.  Envir Research; 38:
   144-154.

Schroeder SR, Hawk B.  (1986) Child  care giver and environmental
  factors related to  lead exposure and IQ.    in:  Schroeder  (ed),
  Toxic Substances and Mental Retardation;  Neurobehavioral Toxicoloqv
  and Teratology;(in press).

Schwartz J, Angle C, Pitcher H. (1986) The relationship between
  childhood blood lead levels and stature.  Pediatrics; 77: 281-288.

-------
                                -30-
Schwartz J, Janney A, Pitcher H. (1984b) The relationship between
  gasoline lead and blood lead. U.S. EPA, Office of Policy Analysis.

Schwartz J. (1985) The relationship between blood lead and blood
  pressure.  Presented at the International Conference on Heavy
  Metals in the Environment. September; Athens, Greece.

Schwartz J and Otto D. (1987) Blood lead levels, hearing thresholds,
  and neurobehavioral development in NHANES II children and youth.
  Archives of Environmental Health — in press.

Seattle Water Metals Survey. (1978) Prepared by Courchene et al.
  and presented to the Seattle King County Health and Water Depart-
  ments and U.S. EPA, Region 10.

Shah BV.   (1982) SURREGR; Standard Errors of Regression Coefficients
  from Sample Survey Data. Research Triangle Park, NC, Research
  Triangle Institute.
Shaper AG, Packham RF, Pocock SJ. (1980) The British Regional Heart
  Survey:  Cardiovascular mortality and water quality.  Journal of
  Environmental Pathology and Toxicology; 4 (2 & 3): 89-112.
Sharrett AR, Carter AP, Orheim RM, Feinleib M.  (1982a) Daily intake
  of lead, cadmium, copper and zinc from drinking water:  the
  Seattle study of trace metal exposure.  Environmental Research;
  28: 456-475.

Sharrett AR, Orheim RM, Carter AP, Hyde JE, Feinleib M. (1982b)
  Components of variation in  lead, cadmium, copper, and zinc concen-
  tration in drinking water:  the Seattle study  of trace metal
  exposure.  Environmental Research;  28: 476-498.

Sharrett AR, Morin MM, Fabsitz RR, Bailey KR.  (1984) Water hardness
  and cardiovascular mortality. In Bell and Doege (eds):  Drinking
  Water and Human Health; American Medical Association.

Sheiham I, Jackson PJ.  (1981) The scientific  basis  for control  of
  lead in drinking water by water treatment.  Journal of the Institute
  of Water Engineers and Scientists;  35(6): 491-515.

Shier DR, Hall A.  (1977) Analysis of  housing  and data collected in
  a lead-based paint survey  in Pittsburgh. National Bureau of
  Standards.

Shlossman M, Brown M, Shapiro E, Dziak R.  (1982) Calcitonin effects
  on  isolated bone cells. Calcif Tissue Int;  34: 190-6.

-------
                                -31-
Silbergeld EK, Adler HS. (1978) Subcellular mechanisms of lead neuro-
  toxicity. Brain Research; 148: 451-67.

Silbergeld EK, Hruska RE, Bradley D, Lamon JM, Frykholm BC. (1982)
  Neurotoxic aspects of prophyrinopathies: lead and succinylacetone.
  Environmental Research; 29: 459-471.

Silbergeld EK, Hruska RE, Miller LP, Eng N. (1980) Effects of lead
  in vivo and in vitro on GABAergic neurochemistry. J Neurochem;
  34: 1712-8.

Silbergeld E and Schwartz J. (1986) Mobilization of bone lead in
  women. Presented at: American Society for Pharmacology and
  Experimental Therapeutics/Society of Toxicology Conference.
  Baltimore, Md; August.

Silver W, Rodriguez-Torres R. (1968) Electrocardiographic studies
  in children with lead poisoning. Pediatrics; 41: 1124-7.

Singh NP. (1979) Intake of magnesium and toxicity of lead:  An
  experimental model. Archives of Environmental Health;
  34: 168-172.

Singhal PL, Thomas JA eds. (1980) Lead Toxicity. Urban and
  Schwartzenberg, Inc; Baltimore.

Six K and Goyer R. (1970) Experimental enhancement of lead toxicity
  by low dietary calcium. J Lab Clin Med; 76(6): 933-942.

Six K and Goyer R. (1972) The influence of iron deficiency on
  tissue content and toxicity of ingested lead in the rat. J Lab
  Clin Med; 79(1): 128-136.

Smith CM, De Luca HF, Tanaka Y, Mahaffey KR. (1981) Effect of lead
  ingestion on functions of vitamin D and its metabolites.  J Nutr;
  111: 1321-1329.

Smith M, Delves T, Lansdown R, Clayton B, Graham P. (1983) The
  effects of lead exposure on urban children: the Institute of
  Child Health/ Southampton study.  United Kingdom Department of
  the Environment.                         \
                                            \
Smith RS. (1974) The feasibility of an injuryXtax approach to
  occupational safety. Law and Contemporary Problems; 38: 730-44.

Smith RS. (1976) The Occupational Safety and Health Act. Washington,
  DC: American Enterprise Institute for Public Policy Research.

Sorrell M, Rosen JF, Roginsky M. (1977) Interactions of lead, calcium,
  vitamin D, and nutrition in lead-burdened children.  Archives of
  Environmental Health; p. 160-164.

-------
                                -32-
Standard Methods for the Examination of Water and Waste Water.
  (1971, thirteenth edition).  Published jointly by the American
  Public Health Association, American Water Works Association,
  and Wafcer Pollution Control Federation; Washington, B.C.

Tera, et al. (1985) Identification of gasoline lead in children's
  blood using isotopic analysis. Arch Env Health; January.

Thaler R, Rosen S. (1976) The value of saving a life: evidence from
  the labor market. Taleckji NE ed. Household Production and Consump-
  tion. Columbia University Press, New York.

Thomas HF, Elwood PC, Tuthill C, Morton M. (1981) Blood and water
  lead in a hard water area.  The Lancet; May; p. 1047-1048.

Thompson NG, Sosnin HA.  (1985) Corrosion of 50-50 tin-lead solder in
  household plumbing. Welding Journal; April; p. 20-24.

Trefry JH, Metz S, Trocine RP, Nelsen TA. (1985) A decline in lead
  transport by the Mississippi River. Science; 230: 439-441.

Treweek GP, Glicker J, Chow B, Sprinker M. (1985) Pilot-plant
  simulation of corrosion in domestic pipe materials. JAWWA; October;
  p. 74-82.32

U.S. Department of Health, Education, and Welfare. (1973a) Limita-
  tions of activity and mobility due to chronic conditions. Public
  Health Service, Vital and Health Statistics Series 10, (96).

U.S. Department of Health, Education, and Welfare. (1973b) Preva-
  lence of selected chronic respiratory conditions:  United States
  - 1970.  Public Health Service, Vital and Health Statistics
  Series 10; (84).

U.S. Environmental Protection Agency. (1977) Survey of Operating
  and Financial Characteristics of Community Water Systems. (GPO);
  Washington, D.C.; April.

U.S. Environmental Protection Agency. (1982a) 1982 NCLAN Annual
  Report.  Environmental Research Lab; Corvallis, Oregon.

U.S. Environmental Protection Agency. (1982b) Corrosion in Potable
  Water Systems. Prepared by DW DeBerry et al. of SumX Corporation
  for the Office of Drinking Water; February.

U.S. Environmental Protection Agency. (1982c) Manual for the Certi-
  fication of Laboratories Analyzing Drinking Water.   (Criteria,
  Procedures, Quality Assurance).  Office of Drinking Water; October.

-------
                                -33-
U.S. Environmental Protection Agency. (1984) Corrosion Manual for
  Internal Corrosion of Water Distribution Systems.  Prepared by
  Environmental Science and Engineering, Inc.(ed: Singley et al.)
  for the Office of Drinking Water.

U.S. Environmental Protection Agency. (1984a) Technologies and
  Costs for the Removal of Lead from Potable Water Supplies.
  Prepared by Ciccone and Associates for the Office of Drinking
  Water; October 23; Final draft.

U.S. Environmental Protection Agency, Office of Policy Analysis.
  (1984b) Preliminary Regulatory Impact Analysis of Proposed Rules
  Limiting the Lead Content of Gasoline; July 23.

U.S. Environmental Protection Agency. (1984c) Regulatory Impact
  Analysis Guidelines; Office of Policy Analysis.

U.S. Environmental Protection Agency. (1985a) Occurrence of Lead
  in Drinking Water, Food and Air.  Prepared by JRB Associates for
  the Office of Drinking Water; January.

U.S. Environmental Protection Agency. (1985b) The Costs and Benefits
  of Reducing Lead in Gasoline.  Prepared by Schwartz J, Pitcher H,
  Levin R, Ostro B, Nichols AL; Office of Policy Analysis.

U.S. Environmental Protection Agency. (1986) Air Quality Criteria
  Document for Lead. Environmental Criteria and Assessment Office
  (ORD); March. This includes The Addendum to the Criteria Document,
  which is appended to Volume 1.

U.S. Environmental Protection Agency. (1986a) Methodology for Valuing
  Health Risks of Ambient Lead Exposure. Prepared by Mathtec, Inc.,
  for the Office of Air Quality Planning and Standards.

U.S. Environmental Protection Agency. (1987) Internal Corrosion in
  Drinking Water Distribution Systems:  A Review of EPA's Research
  Activities. Preliminary draft.  Water Engineering Research Labora-
  tory (ORD); Cincinnati, Ohio; January.

U.S. Office of Management and Budget. (1981) Interim Regulatory
  Impact Analysis Guidance; p. 4.

Victery W, Vander AJ, Markel H, Katzman L, Shulak JM, Germain C.
  (1982a) Lead exposure, begun in utero, decreases renin and angio-
  tension II in adult rats. Proc Soc Exp Biol Med 170: 63-67.

Victery W, Vander AJ, Shulak JM, Schoeps P, Juluis S. (1982b) Lead,
  hyper-tens ion, and the renin-angiotens.in system in rats. Journal
  Lab Clin Med; 99: 354-62.

Victery W, Vander AJ, Schoeps P, Germain C. (1983) Plasma renin
  is increased in young rats exposed to lead in utero and during
  nursing.  Proc Soc Exp Biol Med; 172:  1-7.

-------
                                -34-
Vimpani GVf Wigg NR, Robertson EF, McMichael AJ, Baghurst PA.
  (1985) The Port Porie Cohort Study:  blood lead concen-
  trations and childhood developmental assessment.  Presented at:
  Lead Environmental Health: the current issues. Duke University;
  North Carolina; May.
Violette, Chestnut. (1983) Valuing Reductions in Risks:
  of the Empirical Estimates.
A Review
Viscusi WK. (1978) Labor market valuations of life and limb: empirical
  evidence and policy implications. Public Policy; 26s 359-86.

Wade WA III, et al. (1975) A study of indoor air quality. J Air
  Pollut Control Assoc; 25: 930-939.

Walker R, Oliphant R. (1982a) Corrosion of lead in drinking water.
  Anti-Corrosion (a British journal); April; p. 8-11.

Walker R, Oliphant R. (1982b) Contamination of potable water from
  lead-based solders.  Anti-Corrosion (a British journal); July;
  p. 13-15.

Webb RC, Winquist RJ, Victery Wf Vander AJ. (1981) In vivo and in
  vitro effects on lead on vascular reactivity in rats. Am J Physiol;
  24: H211-6.

Wedeen RPf Maesaka JK, Weiner B, Lipat GAf Lyons MM, Vitale LF,
  Joselow MM. (1975) Occupational lead nephropathy. American Journal
  of Medicine; 59: 630-41.

Weiss ST, Munoz A, Stein A, Sparrow D, Speizer FE. (1986) The
  relationship of blood lead to blood pressure in a longitudinal
  study of working men.  American Journal of Epidemiology; 123:
  800-808.

Weinstein MC, Stason WB.  (1977) Allocation of resources to manage
  hypertension. New England Journal of Medicine; 296(13): 732-9.

Weston RS.  (1920) Lead poisoning by water and its prevention.
  Journal of the New England Water Works Association; volume 34.

White JM, Harvey DR. (1972) Defective synthesis of A and B globin
  chains in lead poisoning. Nature  (London); 236:  71-3.

Wibberly DG, Khera AK, Edwards JH, Rushton DI. (1977) Lead levels
  in human placentae from  normal and malformed births. Journal of
  Medical Genetics; 14: 339.

Williams BJ, Griffith WH  III, Albrecht CM, Pirch JH, Hejtmancik MR
  Jr. (1977) Effects of chronic lead treatment on some cardiovascular
  responses to norepinephrine in the rat. Toxicology Appl Pharma-
  col; 40: 407-13.

-------
                                -35-
Williams BJ, Goldman D, Hejtraancik MR, Ziegler MG. (1978) Nor-
  adrenergic effects of lead in neonatal rat. Pharmacology; 20(3):
  186.

Williams BJ, Hejtmancik M. (1979) Time and level of perinatal
  lead-exposure for development of norepinephrine cardiotoxicity.
  Res Comm CP; 24(2): 367-76.

Williams BJ, Hejtmancik MR, Abreu M. (1983) Cardiac effects of lead.
  Fed Proc Fed Am Soc Exp Biol; 42: 2989-2993.

Winneke G, Brockhaus A, Baltissen R. (1977) Neurobehavioral and
  systemic effects of long-term blood lead elevation in rats. Arch
  Toxicol; 37: 247-63.

Winneke G. (1979) Impaired intelligence in children from environ-
  mental lead (letter). Mun Med Woe; 121(26): 865.

Winneke G, Lilienthal H, Werner W. (1982a) Task dependent neuro-
  behavioral effects of lead in rats. Arch Toxicol; Supp 5: 84-93.

Winneke G, Hrdina KG, Brockhaus A. (1982b) Neuropsychological
  studies in children with elevated tooth-lead concentrations.
  Part 1: pilot study. Int Arch Occupational and Environmental
  Health; 51: 169-83.

Winneke G, Kramer U, Brockhaus A, Ewers U, Kujanek G, Lechner H,
  Janke W.  (1983) Neuropsychological studies in children with
  elevated tooth lead concentrations.  Part II:  extended study.
  Int Arch Occup Environ Health; 51: 231-52.

Winneke G, Beginn U, Ewert T, Havestadt C, Kramer U,  Krause C,
  Thron HL, Wagner HM. (1984) Studie zur erfassung subklinischer
  bleiwirkungen auf das nervensystem bei kindern mit bekannter
  pranataler exposition in Nordenham. [Study on the determination
  of subclinical lead effects on the nervous system of Nordenham
  children with known pre-natal exposure.]  BGA-Berichte.

Winneke G, Beginn U, Ewert T, Havestadt C, Kraemer U, Krause C,
  Thron HL, Wagner HM. (1985a) Comparing the effects of perinatal
  and later childhood lead exposure on neuropsychological outcome.
  Environ Res; 38: 155-167.

Winneke G; Brockhaus A, Collet W, Kraemer U, Krause C, Thron HL,
  Wagner HM. (1985b) Predictive value of different markers of lead-
  exposure for neuropsychological performance. In:  Lekkas TD, ed.
  International conference: Heavy Metals in the Environment;
  September; Athens, Greece,  v. 1. CEP Consultants, Ltd; Edinburgh,
  United Kingdom; pi 44-47.

Wolf AW, Ernhart CB, White CS. (1985) Intrauterine lead exposure and
  early development. In: Lekkas, TD, ed. International conference:
  Heavy Metals in the Environment; September; Athens, Greece, v. 2.
  CEP Consultants, Ltd; Edinburgh, United Kingdom; p. 153-155.

-------
                                -36-
Wolman A. (1986) Notes and comments on Hudson and Gilcreas (1976).
  Journal of the AWWA; 68: 216-217.

Wong, CS, Berrang P.  (1976) Contamination of tap water by lead
  pipe and solder.  Bulletin of Environmental Contamination and
  Toxicology; 15(5):  530.

Wong GL. (1983) Actions of parathyroid hormone and 1,25-dihy-
  droxcholecalciferol on citrate decarboxylation in osteoblast-like
  bone cells differ in calcium requirement and in sensitivity to
 "trifluoperazine.  Calcif Tissue Int; 35: 426-31.

World Health Organization, United Nations Environmental Program.
  (1977) Lead; Environmental Health Criteria 3; Geneva, Switzerland.

Worth D, Lieberman M, Karalekas P, Craun G. (1981) Lead in drinking
  water: The contribution of house tap water to blood lead level.
  Lynam et al.  (eds), Environmental Lead. Academic Press, p. 199-
  225.

Yankel A, Von Lindern J, Walter S. (1977) The Silver Valley lead
  study: The relationship between childhood blood lead levels and
  environmental exposure. J Air Pollut Control Assoc; 27: 763-767.

Yip R, Norris TN, Anderson AS. (1981) Iron status of children with
  elevated blood  lead concentrations. Journal Pediatr (St. Louis);
  98: 922-5.

Yule W, Landsdown R,  Millar IB, Urbanowicz MA.  (1981) The relation-
  ship between  blood  lead concentrations,  intelligence and attainment
  in a school population: A pilot study. Dev Medical Child Neurology;
  23: 567-76.

Yule W, Lansdown  R.  (1983) Lead and children's development: recent
  findings. Presented at  international conference: Management and
  Control of Heavy Metals  in the Environment; September; Heidelberg,
  West Germany.

Yule W, Urbanowicz MA, Lansdown R, Millar  IB.  (1984) Teacher's
  ratings of children's behaviour  in  relation  to  blood lead levels.
  British Journal of  Developmental Psychology.

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             APPENDIX As  BOSTON CASE STUDY
THE COSTS AND BENEFITS OF TIGHTENING  THE  MAXIMUM CONTAMINANT
LEVEL FOR LEAD IN DRINKING WATER FROM .05 MG/L TO .01 MG/L:
           A CASE STUDY OF BOSTON,  MASSACHUSETTS
                 A Policy Analysis Exercise
                        Submitted in
          Partial Fulfillment of the Requirements
          for the Masters in Public Policy Degree
      Kennedy School of Government, Harvard University
                     Jonathan Jacobson
                       April 14, 1986

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                      TABLE OF CONTENTS








EXECUTIVE SUMMARY 	 	  page i




 INTRODUCTION 	„	  Paqe 3




BACKGROUND	  Pag* 5




BOSTON:  ITS WATER AND CURRENT TREATMENT 	 Page  12




PROPOSED TREATMENT AND ITS COST 	 Page  15




HEALTH BENEFITS  	 page  20




CHILDREN'S BENEFITS 	 page  22




HEALTH BENEFITS  — ADULT  WHITE MALES, AGES 4O-59  ... Page  26




           Hypertension	 Page  28




           Cardiovascular  Disease	 Paqe  28




               Myocardial  Infarctions.	 Page  29




               St r okes	 Page  30




               Deaths	 Page  30




           Total  Benefits  for  Adult  White Males 	 Page  31



MATERIALS  BENEFITS	Page  33




RESULTS AND  DISCUSSION	 Page  36



RECOMMENDATIONS  	 Page  40

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 EXECUTIVE SUMMARY








     This paper reports  the  findings of the cost/benefit analysis




 of  lowering the maximum  contaminant level  (MOD  for  lead in




 drinking  water  to .01 mg/L using the City of Boston  as a case



 study.  After discussing the problem of corrosion related lead




 contamination in  general terms and for Boston in particular, my




 study  estimated the  costs of additional corrosion control




 required  to lower lead levels in Boston to the contemplated




 standard, the health benefits resulting from the lower lead




 levels, and- the benefits of  reduced materials damage produced by




 the additional  treatment of  drinking water.




     Although rny  analysis generated results under different




 assumptions, the  net  benefit for the most lively case is




 $7,200,000 Ci985$:) in  1988 rising to *8,000,000 in 1992.   The




 Boston share of treatment  costs  in 1988 is $7OO,000.   On the




 benefits side,  the analysis  yielded the following estimates in



 1988:




                $340,000  for  children's health effects,




                $190,OOO  for  avoided myocardial  infarctions,



                $115,OOO  for  avoided strokes,




               $6,300,000  for  avoided  deaths,  and




                $940,000  for  reduced materials damage.




 In terms of benefit/cost ratios,  the results  are 11.5:1  in  1988




rising to 12.7:1  in  1992.  Population  growth  in  Boston  accounts



for  the steady rise  in health  benefits  throughout the period.

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                                2


     In order to account for uncertainties and statistical biases

resulting from both the data employed in the analysis and the

exclusion of important categories of health effects  Ce.g. renal

damage, pregnancy complications, and cardiovascular  disease in

other age groups and in blacks), sensitivity analysis was

performed.  Even under a pessimistic set of assumptions,

additional treatment would still yield positive net  benefits.

Using optimistic assumptions, the case for lowering  the MCL for

lead is overwhelming (net benefits = $11.5 million in 1988).

     The results of the analysis suggest that EPA should take the

following actions:
               1. Lower the maximum contaminant level
                  for lead from .05 mg/L to .01 mg/L.
                  The agency should consider waivers in
                  exceptional cases.

               2. Provide technical assistance and
                  information to localities to aid them
                  in their efforts to control corrosion
                  thereby reducing levels of lead and
                  other contaminants in drinking water.

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 INTRODUCTION








      Sine* Roman times, people  have  known  about  some of the toxic




 effects of human exposure to  lead.   Despite these concerns,  lead




 has continued to be used for  a  variety  of  purposes:  as an




 additive in paint and gasoline  and as a material  for water




 conveyance pipes.  It was not until  recently,  however,,  that




 governments have taken action to reduce environmental  exposure to




 lead.   In the United States,  the use of lead based paint  was




 banned.   The federal government also regulated the use  of lead as




 an  additive in gasoline beginning in the early 1970s.   Among




 toxic  substances,  lead was one of the first for which exposure



 standards were established.




      Increasingly,  research  has indicated that physiological  and




 neurophysiological  damage  can r/..-3ult  from exposure to levels




 previously thought  to be safe.  In light of this evidence, the




 Centers  for  Disease Control  CCDC)  lowered the criteria  for lead




 poisoning  in  children  from 3O pg/dl  to 25 jjg/dl Cwhen coupled




 with free  erythrocyte  protoporphyrin  CFEP:>  of 35 pg/dl).  It has




 motivated  the  EPA to  propose a phase  out  of the use of leaded




 gasoline.   In  response  to the growing concern about low-level




 exposure to lead, EPA  also has proposed  that the  MCL for lead be



 lowered to  .01 mg/L.




     While lead can be  found  in  both  ground and surface water




supplies, the  major source  of contamination of drinking water is




the leaching of lead from water  distribution pipes and household

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plumbing by corrosive water.*   Treatment  methods now being used

in some communities have reduced  lead  concentrations below the

current MCL of .05 mg/L.   If a  new,  lower standard is adopted,

though, additional treatment may  be  required  even in communites

currently undertaking treatment.

     As part of the regulatory  process, the agency has examined

the costs and benefits of  water treatment for  the country as a

whole.  To corroborate these analyses  and examine the costs and

benefits in a more systematic fashion,  the Office of Policy

Analysis has undertaken case studies of several  cities.   As a

part of this effort, I was asked  by  that  office  to perform a

cost/benefit analysis for  Boston,  a  city  which has highly

corrosive water and whose  water distribution  system is

representative of older urban areas.

     After describing t!,e  general  problem of  lead and corrosion

and potential treatment methods,  this  study will look at Boston's

situation and its history  of corrosion control.   The analysis

itself will begin with an  examination  of  the  additional  treatment

likely to be employed in Boston and  its cost.   It will then turn

to the benefits.  Because  of data and  epiderniological

constraints, the benefits  analysis is  limited  to avoided costs

associated with neurological damage  in children, hypertension and

related cardiovascular disease  in adult white  males,  aged 40-59,

and reduced materials damage.   This  paper will conclude with a
i U.S. Environmental Protection  Agency,  "Regulating Corrosive
Water", Office of Planning and Evaluation,  April  1981,  p.2.

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 comparison  and discussion of the costs and benefits and

 r ec ommendat i ons.



 BACKGROUND
      The problem  at  hand stems from the unfortunate coincidence

 of highly corrosive  water  and the use of piping materials

 containing substances  which,  when leached, contaminate drinking

 water.   While this analysis  is primarly concerned with the health

 impacts of lead and  general  materials damage, corrosive waters

 may also contribute  other  substances including, cadmium,

 asbestos,  iron,  and  copper to drinking water.

           Despite our  longstanding  knowledge that lead is harmful

 to human health, several characteristics have made it  popular as

 a  material  for water piping.   It  is  easy to  form,  cut  and join.

 It is also  durable and resistant  to  subsidence and frost.*

 Because of  its durability,  many lead pipes installed  in  the early

 part  of this  century are still in use.   In addition, a number of

 building codes still  allow its use for  joining conveyance pipes.=>

      Lead can  be found  at many points between  the  water  source

 and the consumers'  tap.  Although utilities once used  lead  lined

 water mains, many  of  these  have been replaced.  Currently,  a

 major source of  concern is  the use of lead in  sevice lines, the

 2 American Water Works  Association CAWWA) , Internal r:.-,rr,-.^-i .-,» ,-,f
Water Distribution  Systems;  Cooperative Research Reoor~1985.  p.


 3 U.S.  EPA,  "Statement  of Basis and Purpose for Amendments  tr, the
National Interim Primary  Drinking  Water Requl at i .-ins"  Of fire  r,f
Drinking Water,  198O, p.  48.     "                      urn.e  ... r

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piping which connects a building's  plumbing  with  the main.   While

many of these pipes have been  replaced  over  the years,  a large

number remain in use.  Lead  can  also  be found in  goosenecks,

caulking, gaskets, solder and  plumbing  fixtures.-*

     Although solder and plumbing  fixtures constitute

proportionally a small amount  of interior  surface area,  studies

have shown that these sources  can contribute a significant

proportion of the  lead found in  drinking water.    A British

study in 1977 found lead levels  in  houses  without lead pipes as

high as those found in lead  plumbed houses.3  These results were

confirmed by a second study  by Lyon and Lenihan who collected

water samples from a modern  office  building  with  lead based

solder but no lead plumbing.   Forty four percent  of the samples

exceeded .1 mg/L.* Studies  also show that while lead levels

decrease rapidly with the age  of the  soldered joints,

contamination will persist  for many years.17  Laboratory studies

have corroborated  these  findings and  have  also demonstrated

analogous problems for brass and bronze plumbing fixtures.0

     These results are a cause of  concern.  While the incidence

of lead in service lines, mains, and  internal plumbing has
4 Karalekas, P.  et  al.,  "Lead  and Other Trace Metals in Drinking
Water in the Boston Metropolitan Area", Proceedings AWWA 95*ti%
Annual Conference,  Minneapolis,  Minnesota,June 9-12, 1975, p. 7.

5 AWWA, OP. cit.. p. 215

& Ibid., p.216

7 Murrell, Norman,  "Impact  of  Metallic Solders on Water Quality",
Specialty Conference on  Environmental  Engineering, EE Division,
ASCE/Boston, MA,  July 1-5,  1985.

8 AWWA, Qp. cit.. p. 222

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 declined,  the vast  proportion of building plumbing systems  still

 use  lead-based solder.   This fact suggests that lead may  be a

 problem wherever  water  is corrosive,  not only in older urban

 areas where  lead  plumbing and service lines can still be  found.

 In fact, newly soldered  joints will  contribute lead even  in areas

 where water  supplies  are not  corrosive.

      The other  part of the  problem  is corrosive drinking water

 supplies.   A  large number of  water  utilities supply corrosive

 wa,ter.    In two studies,  one  by  Millette and the other  by the

 Midwest Research  Institute  CMRI), over  two-thirds  of  the

 utilities  sampled reported  distributing  water  that  is either

 moderately or highly corrosive.   Millette's  study  examined 130

 utilities  serving more than 40 million people.   The MRI  sample

 included 388 utilities serving more than  103 million  people.*

      A  number of factors contribute to the corrosive  nature  of

 water.. Among them are low PH, alkalinity, hardness,  dissol-ed

 oxygen, dissolved  solids, velocity and temperature. 1<:>

 Contaminant  levels are also greatly affected by the length of

 time  that the water  is in contact  with sections of pipe.  When

 water has been standing  in the service line and internal

 plumbing, it  tends to  produce higher levels of contaminants. »«•

An important  characteristic  that  affects corrosivity is the

hardness of water,  that is,  the concentration of calcium

9 U.S. EPA, "Statement of Basis and  Purpose for Amendments tn the
National Interim Primary  Drinking Water  Regulations",   pp.37-4O.

10 U.S.  EPA,  "Regulating  Corrosive Water",  p.3.

11  U.S.  EPA, "Statement of Basis  and Purpose  for  Amendments  bn
the National Interim Primary Drinking  Water Regulations",   p.31.

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                                a


carbonate CCaCOa).  In hard waters, where  high  concentrations of

CaCOs are present, a protective skin  forms along  the inner  walls

of pipes. •» =  Soft water tends to be corrosive because the CaCQ3

concentration is low which inhibits the  formation of the

protective film. JS

          Before discussing the various  methods currently

available to lower lead levels, I  would  like to briefly discuss

the kinds of health effects associated with exposure to lead.

Lead has long been implicated for  its damage to the brain and the

central nervous system.  At low-level exposure, the concern is

especially great for children who  retain proportionally greater

amounts of lead and who are also going through  critical stages in

the development of the brain and cognitive abilities,  making

them even more vulnerable.1"*   Studies show that  exposure to lead

may cause anemia and renal damage;  at high levels, it can result

in encephalopathy and death.1"  Researchers have  also

demonstrated a negative relationship  between blood lead levels

and IQ.   In addition, epidemiological studies  have demonstrated a

relationship between elevated lead levels  in pregnant women and

low-level fetal malformations.  Elevated blood  lead levels in

pregnant women also may lead to still births  and  miscarriages.1*
 12  Ibid., pp.31-32

 13  Ibid., p.35

 14  U.S.  EPA.  "Regulating Corrosive Water",  1981,p.6.

 IS  Ibid., p.S.

 16  U.S.  EPA,  Costs and Benefits of Reducing Lead in Gasoline,
 1385,  chapter  IV.

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                                  '=!


       Studies from the mid-1970's have suggested  uhat  there is a

  relationship between soft water and cardiovascular  disease CCVD.') .

  While some  evidence indicates that the mechanism  for  this is soft

  water's deficiency in magnesium and calcium, substances  that may

  have a protective effect  on blood pressure, leachate  contaminants

  common is soft  water  such as lead can increase blood  pressure,

  and with it,  the  incidence of CVD. *»•  In fact,  epidemiologists

  have uncovered  a  very strong relationship between blood  lead

 levels and blood  pressure.   According to a study by Pirkle et

 al . ,   a 377. drop  in blood  lead was  associated with a  17.5%

 reduction in cases of  hypertension-  and  lower rate of CVD.1*

      Short Of the wholesale  replacement  of distribution pipes,

 water utilities can lower  lead  concentrations by controllina

 corrosion.   Control techniques  currently  used  include pH

 adjustment,  hardening, and the  addition of  silicates or

 phosphates.   The choice of method depends  upon  both  the

 characteristics of the water and the types  of materials used  in

 the distribution system. 1<9

      Adjusting pH is a widely used method to treat corrosive

 water.  Most  utilites that adjust pH use lime.   In addition  to

 raising pH,  lime increases alkalinity and the hardness of water.

The high concentration of  calcium promotes the  formation  of the

 17 U.S. EPA,  "Statement of Basis and Purpose for Amendments t,-,
the National  Interim  Primary Drinking Water Regulations",  p.45.

 IS Pirkle et.  al.,  "The Relationship Between Blood Lead Levels
and Blood Pressure and its Cardiovascular  Risk  Implications",
American Journal of Epi derneol ogy,  1385,  121:245

19 U.S. EPA,   "Statement of  Basis and Purpose for Amendments tr,
the National   Interim Primary  Drinking Water Requl at i nns"   D '-'&
                                     "          —      —>—'»f-/« 4» \*j m

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                                10


protective CaCOa film.  With respect  to  vhe  dissolution  of  lead,

pH adjustment facilitates the  formation  of an  insoluble  lead

precipitate that adheres to the  inner walls  of pipes and prevents

metallic lead from being further attacked.30  The  American  Water

Works Association CAWWA) cites  laboratory studies  indicating  that

lead dissolution approaches a  minimum when pH  approaches 9.21

     Corrosion can also be controlled with the use of corrosion

inhibitors (e.g. sine orthophosphate), chemical  additives which

help form a protective  film.   While phosphate  treatments have

been used for over a decade, intensive research has taken place

in only the last several years.  These studies indicate  that

treatment with sine orthophosphate  is effective,  but only within

certain pH and alkalinity constraints.a:z

     Aside from lowering lead  concentrations,  corrosion  control

has lowered the levels  of other  contaminants and reduced  damage

to water pipes and other distribution system components.  As a

result, any analysis' of the costs and benefits of  corrosion

control must not only consider  the  benefits  from reduced exposure

to lead but also from the reduced exposure to  other contaminants,

avoided materials damage and improved aesthetics.

     Cadmium, another material  found  in  distribution pipes and

leached by corrosive water  is  also  linked  to hypertension.    It is

found at high levels in hypertensives and  has induced
20  Karalekas,  "Alternative Methods for Controlling the
Corrossion of Lead  Pipe",  Journal  of the New England Water Works
Association, June  1978,  p.2.

21 AWWA, op. c i t.,  p.243

22 Ibid.. pp.246-260.

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                                 11


 hypertension  in  animal  studies.^  Cadmium also may cause

 irreversible  renal  damage.35"*  Concern also has been expressed

 over the use  of  asbestos lined concrete pipes.  While asbestos is

 a known carcinogen  when  inhaled,  its health effects when ingested

 have not been well  defined.3"5   Because asbestos pipe is not used

 in Boston and cadmium levels are  acceptably low,  contamination

 from these substances was not  examined in  this analysis.

      In addition to the  contaminants  regulated by primary

 standards,  there are substances subject  to secondary standards

 that also are leached from pipes.  These include  iron  and copper.

 EPA regulates copper on  the basis of  smell  and taste.

 Concentrations greater than the 1 mg/L standard may  also  stain

 sinks and porcelain.  Likewise, iron  is also regulated on the

 basis of  aesthetic  considerations.aa

      Finally,  corrosive water damages pipes and other components

 with  which  water  comes in contact.   The process of  leaching

 minerals  causes more rapid interior degradation of both

 distribution pipes  and privately owned plumbing pipes, making

 them  more susceptible  to  leakage and  rupture.*"  Leakage  from

 distribution systems may  be  substantial,  sometimes accounting  for
23 U.S. EPA,  "Regulating  Corrosive Water",  p.8.

24 U.S. EPA,  "Statement of  Basis  and  Purpose for Amendments to
the National  Interim Primary  Drinking Water Regulations",  p.  44.

25 U.S. EPA,  "Regulating  Corrosive Water",  p. 8.

2& Bureau of Water Works, Por 11 and , Or egon ,  Internal  Corr-nsi nn
Mitigation Study; Final Report, 1382.  p . 5-12.  ""

27 U.S. EPA, "Regulating  Corrosive Water",  p.13.

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                                12


337. of the water supply.=•   In  addition,  corrosion promotes

tuber.= ulat ion, a process in  which leached materials build up on

the inner walls of pipes reducing their  carrying capacity.a9

This deterioration leads to  reduced  flow and the need to increase

pumping on the part  of  the utility.   Various studies have shown

that the costs of corrosion  damage are substantial.



BOSTON;  ITS WATER  AND CURRENT TREATMENT
     The water supplied  to  Boston by the Massachusetts Water

Resources Authority  CMWRA),  the regional 'wholesale' water

utility, is among  the  most  corrosive in the country.  It is

relatively acidic  with a pH of 6.7,  and soft with hardness

measured at 12 mg  CaCQa/L.   Alkalinity is,low as well.30  Boston

is also a city with  an old  distribution system and housing stock

and has a significant  number of lead services still in existence.

Although local officials have long recognised the dangers

inherent in the  use  of lead pipe for supplying potable water  and

have commenced the systematic replacement of lead services,

property owners  are  responsible for  that portion of the service

line that runs from  the property line to the structure.  As  a

result, staff engineers at  the Boston Water and Sewer Commission
28 U.S.  EPA,  "Statement of Basis and Purpose  for Amendments  to
the National  Interim Primary Drinking Water Regulations",  p.27.

29 U.S.  EPA,  Regulating Corrosive Water, p.13.

3O Karalekas  et.  al . ,  "Control of Lead, Copper, and  Iron  Pipe
Corrosion", Journal  of the American Water Works Association,
1933,  p.93.

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                                 13


 t'BWSC) estimate that 44%  of  their residential customers still

 have lead services.31

      Some studies, however,  indicate that  the lead problem could

 be even more widespread.  The  most  comprehensive tap water

 sampling in Boston indicated that 70% of the household showed

 evidence of lead dissolution.3:*   Since only half the houses in

 the survey had lead services,  we  must  assume that lead is being

 leached out from other sources.   From  the  previous discussion

 concerning lead solder's contribution  to lead levels in drinking

 water,  it  seems likely that solder  accounts for  much of the

 contamination.   Goosenecks and caulking also contribute lead.

      Because of the widespread existence of lead in  piping

 material,  tap water was extensively monitored  in the mid 1970's.

 This  study revealed a large proportion of  samples in excess of

 the .05 mg/L MCL.3=»  In addition,  a study  by  Worth et  al .  showed

 a  statistically significant  relationship between  lead  in  tap

 water and  blood lead  in children.3*  In response  to  this

 situation,  the  Metropolitan  District Commission  CMDC),  the former

 water supply agency,  began treating the region's  water.
31 BWSC staff engineers,  January,  1986.

32 Karalekas, "Lead and Other  Trace Metals in Drinking Water in
the Boston Metropolitan Area",  p.  7.

33 Ibid., p. 13.

34 Worth et. al. "The Contribution of  Household Tap Water to
Blood Lead Levels", U.S.  EPA grant tt R-802794,  1981,  p.20.

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                                14


     At first, the MDC used  sine orthphosphate but  was

unsuccessful.30   CIt now seems  that  the failure of  orthophosphate

was due to the low pH of Boston's  water.3*!)   Beginning in 1977,

the MDC began pH adjustment  using  sodium hydoxide CNaOH:> , a

control technique that has proven  to be extremely effective.  The

MDC chose NaOH over lime because its consultant,  Metcalf and

Eddy,  estimated that capital  and operating and maintenance costs

were significantly lower for  NaOH  treatment.37'  In  addition,

sodium levels in MDC water were sufficiently low that adding

sodium would not create a health problem.3*9

      Monitoring performed by EPA's  Region I office from 1976 to

1981 indicated that lead, iron  and copper levels dropped

significantly.3*  More importantly,  lead levels in  most water

samples fell below  .05 mg/L.   Most  samples, however, had levels

which remain above the contemplated  .01 rng/L MCL.  Ci-.-npl iance

with the proposed standard will require corrosion control to

further reduce lead levels in Boston's drinking water.
p. 94.

36 Discussion with Peter  Karalekas and studies reported in the
AWWA corrosion control  study,  December,  1985.

37 Discussion with Peter  Karalekas,  April,1986.

38 Ibid.

39 Karalekas, "Control  of Lead,  Copper,  and Iron Pipe Corrosion",
p. 93.

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                                 15
  PROPOSED TREATMENT AND  ITS  COST
            The primary objective of additional corrosion control



  is  to reduce lead concentrations in order to comply with the




  proposed  .01 mg/L standard.   Before deciding upon which treatment



  methods would be  appropriate,  we must  first  establish the




  criteria  by  which we  define  compliance with  the standard.   Based



  on  recent  epidemiological  studies and  technical feasibility,  this



  analysis  proposes the  following  compliance criteria.   First,  the



  MCL should be  based on the standing  grab  sample,  that  is,  the




 sample which  is taken  immediately  after turning on  the cold  water




 tap and the one which  is statistically the best  predictor  of




 blood lead levels.  Second, compliance should be  based on  tap



 water collected from a sample of worst case households,  those



 which have new lead soldered .joints, lead servi-es, or  other



 evidence  of lead pipes.  Because it is impossible to guarentee



 that every household  could meet the .01 mg/L standard  even using



 state of  the  art corrosion control techniques, we should use the



 mean concentration generated  by this sample.




      We must  also  be  cognizant  of a number  of uncertainties



 concerning the effectiveness  of corrosion  control techniques.   A



 particular form of treatment  might produce excellent results in



 one  system, and yet, performance  in another may  prove  less



 effective.  In  addition, some  methods have been  extensively



•tested  in  the  lab  but not  in the  field.  The  treatment  methods I



 will discuss  are endorsed by the  new  AWWA  manual  on  corrosion



control.   They  also have been  suggested as the likely

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                                IS


alternatives by engineers at EPA Region  I and the MWRA and have

proven effective in other New England cities where  the

characteristics of the water and the distribution systems are

similar.  Nevertheless, our estimates of expected reductions in

lead concentrations are based only on educated .judgements.

     After reviewing the current research literature on corrosion

control, and discussing the Boston situation with EPA and MWRA

personnel, it is likely that additional treatment would consist

of two stages.-*0 First, MWRA would further raise pH1 by increasing

the NaOH concentration.  When the MDC first began NaOH treatment,

th* state of the art suggested  that pH should be elevated  to a

range of 7 to 8 or higher.  Currently the pH of treated water is

8.5.  Recent findings, however, indicate that corrosion control

will be even  more effective when pH is raised to 9.

     In addition, it is likely  that the utility would take action

to achieve consistent pH levels through-out the complex web of the

MWRA distribution system..  This would necessitate  the

installation of several additional pumping stations to even out

the concentration of NaOH throughout the delivery system.

          While additional and  better controlled pH adjustment

should reduce corrosion, the use of a corrosion inhibitor will

probably be necessary.  Zinc orthophosphate is the  likely

alternative.  Although this method was used unsuccessfully before

in Boston, it now seems that pH was too low.  When  used in a
40 Discussions with Peter Karalekas of EPA and Guy Foss of the
MWRA.  Mr. Foss was reluctant to make any judgments but indicated
that higher pH and zinc orthophosphate was a likely scenario,
December, 1985.

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  higher  pH environment,  corrosion control experts believe that

  orthophosphate will  be  very effective.   In addition, the MWRA

  does  not  expect  a  repeat  of the phosphate induced algae growth

  experienced  in 1976  in  tne smaller storage reservoirs because

  they  are  no  longer used,  a level  that would comply with the

  contemplated MCL."*1


       Like Boston, Bridgeport,  Connecticut  also  has low  pH water

 supplies and widespread use of  lead  in the distribution system.

 Using lime to  raise pH and zinc orthophosphate,  water quality

 authorities in Bridgeport have  successfully  reduced  corrossion.

 Samples for lead indicate a mean concentration  of  .007  mq/L

 overall  and .01 mg/L for the standing grab sample.*»


      The technologies associated with corrosion control  are

 relatively simple and the costs are calculable.   Most treatment

 methods  employ  processes similar bo those used  for chlorination

 and  fluoridation.  The chemicals are held in storage tanks, mixed

 with water, and then  pumped into the distribution system.  Thus,

 the capital component  includes the costs  of storage tanks, mixing

 equipment, pumps  and  installation  labor.   Operating and

 maintenance costs <:O8
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                               is


     The pH adjustment phase of the additional treatment can be

broken down into two components: additional pumping stations and

an increased chemical feed rate.  Because of the low buffering

capacity of Boston's water, only a small increment to the  feed

rate will be necessary to raise the pH to the desired level.

Both the EPA and MWRA estimate that chemical costs would increase

by approximately 105S.  Because NaOH is a by-product of automobile

manufacturing and output varies directly  with automobile  output,

its price has fluctuated dramatically.  Based on the average

price for the last five years, the cost  of NaOH is $.54 per mg

per million gallons  
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                           TABLE  I
                       TREATMENT COSTS
PARAMETERS
average  flow
interest rat*
payback  period
CRF
                         310
                          5'/.
                          20
                     0.08024
NaQH

cost uTig/MG)
feed rate (rng/L)
                         1.4
                                  chemicals
                                     Q&M
                                   capital
                                    total
                                                      $85,541
                                                      $30,000
                                                      $12,036
                                                     $127,578
Zinc Orthoohosohate
EPA  CA)
cost  Crng/MQ)
feed rate  (mg/L)
                       $5.44
EPA <:B>
cost (img/MQ)
feed rate  Crng/L)
                       $5.44
                           3
Tech Products
c ost <•'. mg '.; Zn > /MQ >
f*ed rab*  (mgtZn
                      $21.00
                         0.6
                                  chemicals
                                     O&M
                                   capi tal
                                    total
                                  chemicals
                                     Q&M
                                   cap ital
                                    total
                                                   $1,231,072
                                                      $34,OOO
                                                      $13,641
                                                   $1,278,713
                                                   $1,846,SOS
                                                      $34,OOO
                                                      $13,641
                                                   $1,894,245
                                  chemicals

                                   capi tal
                                    botai
                                                   $1,425,690
                                                      '530, COO
                                                      $12,O36
                                                   $1,467,726

-------
                       TABLE  I  Ccont.)
AWWA
cost  CmgCZn>/MG>      $19.20
feed  rate  Crng CZrO /LJ    O.5
                                   ch emi ca1s
                                      O&M
                                    cap ital
                                     total
*l,08fi,240
   $30,000
   * 12,036
*1, 123,276
                                    'EPA (B.i
                                   TECH PROD
                                    EPA <:A:>
                                      AWWA
$2,021,827
*1, 406,291
* 1,255, 8134

-------
                                19






 uses the figures provided by. Technical Products, a chemical  firm



 which manufactures orthophosphate and supplies the feed systems.



 Assuming a flow of 310 MQD and a feed rate of .6 rng/L, the annual




 chemical cost is $1,425,000 based on a unit cost of $21 per  nig of



 sine per million gallons t.'nig CZn) /MQ).




      The cost of the zinc orthophosphate feed systems are less



 than those for NaOH systems with  a 100 MGD plant costing $30,000.



 In  order to meet peak demand,,  the MWRA would require a total of



 SOO MGD capacity costing * 150,000 or $12,000 on an 'annual  basis.



 Based on these capital  requirements, the expected annual  Q&M



 costs are $30,000.   The total  annual cost for zinc orthophosphate




 treatment is   therefore $1,468,000.   The combined annual  cost of



 pH  adjustment and orthophosphate  is  approximately $1,600,000.



      While  this cost  figure represents the most  likely case,



 there a»-e a number  of factors  which  could lower  treatment  costs.



 First,  Additional  pH  adjustment alone could be sufficient.



 Secondly,  optimal  pH  for  zinc  orthophosphate could require a



 lower  NaOH  feed  rate  and  with  it,  lower  NaOH chemical  costs.



 Finally,  these  costs  are  based upon  MWRA's  projected  demand  of



 310 MGD,  a  forecast which disregards price  responses  
-------
 HEALTH  BENEFITS
      Despite the fact  that  the health effects from exposure to



 lead  are relatively well  understood,  monetising health benefits



 is  complicated  and  requires a number  of stages and several kinds



 of  data.   In graphic terms,  the process is a chain which starts



 with  a  change in contaminant concentration producing a change in



 exposure which  produces  a change in  body lead burden,  which



 finally results in  observable physiological  and neurological



 changes.   By reducing  contaminant  concentrations,  we can reduce



 the adverse  health  impacts  of exposure to lead and avoid the



 various costs associated  with them.



      The first  requirement  of this stage of  the analysis,



 therefore, was  data for  a change in water lead concentration.



 Based on  the definition  of  compliance established  earlier  in  this



 analysis  and the Regi'on  I water  lead  data, we estimated the



 reduction  in lead concentrations.  The mean  concentration  for  the



 standing  grab sample was  .032 mg/L.   This value is based on the



 cross sectional  data pooled  for  the last  five months in which



 samples were taken.  During  this time lead levels  seemed to



 stabilise  following the commencement  of  NaOH treatment.   Since



 compliance by definition  requires  that  we lower  the mean



 concentration to  .01 mg/L,  lead  levels  would drop  by .022  mg/L on



 average.  Assuming  proportional  reductions,  bhe decline in  lead



 concentrations ranges  from  .05 mg/L to  .0055 mg/L.  for  the



households in the sample.

-------
                                21






      Because the sample size is so small, it is  likely  that  this



 reduction in water lead in not representative of tap water



 throughout Boston.  In fact, we know that the houses in the  study



 were selected because they had lead services, a characteristic



 true of only 44% of residential consumers.  The standing draw



 data used here,  though,  is the water that is in contact with



 internal  plumbing.  Because of this fact, the fact that 70% of



 the households surveyed  (only 50% of which had lead service.') in



 1975 showed  evidence of  lead dissolution, and the studies which



 show that lead solder contributes significant amounts of lead to



 drinking  water,  it is likely that the data are representative of




 a much  larger  portion of  the Boston housing  stock.   Therefore, i-n



 the most  likely  case,  this analysis uses a figure of 57% (the



 average of 44% and 70%.") to calculate the number  of houselolds



 effected  by  further  reductions  in drinking water  lead levels.



      Second,  the analysis  required blood lead data for  the



 relevant  segments of  the population,  children and adult  white



 males,  aged  40-59.   In Boston,  only children  are  monitored for



 blood lead.  This data, however,  were not useful  since  it  was



 collected  and  organized for  a completely different  purpose.



 Consequently,  this analysis  employed data from the  National



 Health  and Nutritional Examination Survey CNHANES II>.   By using



national data, however, we are  making the assumption  that  the



 Boston  population groups have the  same blood  lead distribution  as



the nation as a whole.  But  because an  urban population is



 likely  to have blood lead  levels higher  than  the  national



average, the analytical results will be  biased.   The  blood  lead

-------
data also had to be adjusted  for changes  in gasoline  lead  content

so that we can isolate the impact of a change  in  water  lead

concentrations.

     Thirdly, we had to have  population estimates for the  1985-

1995 period.  The population  projections  employed in  this  study

are based on the Census Bureau's estimates and  reveal several

patterns which are significant to this analyis.4*8* Although

Boston's population had declined for most of the  post-war  era,

this trend reversed in this decade.  Population increases  are

most pronounced for the two groups studied in  this analysis.   The

number of young children is expected to grow rapidly  as  the  baby-

boomers start to have children.  In addition,  the ranks  of adult

white males, aged 40-59 will  swell over the newt  decade  as the

baby-boomers age.

     Finally, when estimating health benefits,  this analysis

assumes that the proposed MCL will not be i mpl emented until  at

least 1988.  Thus, the calculations reflect benefits  starting  in

that year and extending out to 1992.



CHILDREN*5 BENEFITS
     In order to calculate the health benefits  for  children,

resulting from reduced exposure to lead in drinking  water,  the

analysis used a methodology similar to that employed  in  EPA's
45 Boston Redevelopment Authority, "Population" Projections  for
Boston and for Boston City Hospital Neighborhoods—by
Race, Ethnici t.y, Age, Income, and Pverty Status—to the  Year  2000,
Research Department, 1S85, pp.41-44.

-------
                                 23


  study  of  lead  in  gasoline.   The derivation of avoided costs is

  based  on  the number  of  children whose blood lead level  falls

  below  25  pg/dl  as the result  of reduced  lead concentrations in

  drinking  water.   We  can  estimate this number by  taking  the

  difference between the number of children  with blood  lead  >25

  pg/dl  at  current  lead levels  in  drinking water and  the  predicted

  number of children with  blood lead  >25 pg/dl  at  lowered  lead

  levels in drinking water.

           In the  first step, children were  broken into  two  racial

 groups, black and non-black, and  into seven  two-year  age groups
                                  •t
  starting with six months to the  second birthday  and ending  with

 twelve to thirteen years of age."**  MIIMITAB, a statistical

 software package,   was then used to generate a distribution of

 blood lead levels for each age/race group based on the parameters

 of the  NHANES II data,  controlling for gasoline lead levels..

      In order to estimate the change in the distribution of blood

 lead  for  each group,  we  had to relate reduced exposure levels as

 measured  by  lower  lead levels in drinking water to blood lead

 levels.   This analysis uses a 19S3 study  by Ryu which  established

 the relationship between  water  lead  and blood lead in  children  as

 depicted  in the  following equation:

                        PbB  =  a  + .12PbW
           where:
               PbB =  blood  lead  in pg/dl;
               a   =  the  constant  plus other  demographic  and
                      other environmental  fact.ors;  and
               PbW =  water lead  in pg/L (standing  grab
                      sarnp lei).
4£ Children Were categorised in this way because blood lead
distributions are heavily dependent on age and race.

-------
                               24






Based on this regression equation and the data on water lead



reduction, a child in Boston is subject to a possible reduction



in blood lead ranging from .£6 pg/dl to £.04 pg/dl depending on



the reduction in water lead in his/her household.



     In the final step, a BASIC program used the initial blood



lead distributions and epidemiological relationship above to



simulate the change in the blood lead distribution for each



aae/race group.  Using the before and after distributions, the



program calculated the probability that a child's blood lead



would drop below 25 pg/dl.  By applying that probability to the



number of children in an age/race group and repeating the process



for all 14 groups, this procedure estimated that additional



treatment of Boston water will reduce the number of lead-poisoned




children by 87 in 19SS  Csee Table 11').



     In terms of medical and compensatory education expenses, EPA



believes that $3,900 can be saved for each avioded case of lead



poisoning: $1,100 for medical treatment and $2,300 for education.



Therefore we can expect a total of $340,000 in benefits  for



children in 1983, rising to $349,000  in 1992.



      This estimate, however, merits  closer scrutiny.  Several



factors suggest that it is somewhat  conservative.  First, the



NHANES  II data probably underestimates blood  lead  levels  for



Boston children.  Urban children are  exposed  to  higher amounts  of



lead  t;automobile exhaust, lead paint, dust, industrial sources)



and are therefore more  likely to have higher  blood  lead  levels.



By using national data, we start out  with proportionally  fewer



individuals with blood  lead  >23 pg/dl thus reducing  the

-------
                                     TABLE II
                              CHILDREN'S  BENEFITS
AMETE8S
jfi; per capita $3,900
.*«? ipphciole 54Z
•G£
•sou?
;-<2yr
2-3
*-5
5-7
5-9
;0-11
:2-l3

POP
4274
5717
5350
4984
4618
4251
2985
v. CHANGE
25 'Jd/dl
0.530Z
0.715Z
0. 70551
0.310Z
0.0857.
0.000%
0.005Z
NUMBER
CHILDREN
12.2
22.1
20.4
3.3
2.1
0.0
0.1
BENEFITS
1388
$47,706
$86,086
$79,433
$32,539
$8,267
$0
$409

POP
4329
5772
5384
4995
4607
4210
3830
SLACKS
BENEFITS
1989
$48,319
$86,914
$79,938
$32,610
$8,247
$0
$.403

POP
4335
5850
5416
5001
4579
4163
3746
BENEFITS
1990
$48,944
$88,089
$80,413
$32,650
$8,197
$0
$394

POP
4390
5855
5467
5078
4690
4292
3907
BENEFITS
1591
$49,000
$88,164
$81,170
$33,152
$8,396
$0
$411

PGP
4396
5861
5495
5143
4784
4422
4070
BENEFITS
1«2
$49,067
$88,254
$81,586
$33,577
$8,564
7
$0
1429
65.2   $254,439
$256,432
$258,687
                                                                   $260,294
$261,477
                                  NON-BLACKS
*SE
;-<2yr
2-3
4-5
5-7
3-9
:o-u
;2-i3
I CHANGE NUMBER
POP 25 ua/dl CHILDREN
7277
9734
'3110
3486
7862
7239
'6615
0. 13SZ
0.1452
O.I20Z
0.0652
O.OOOZ
0.0002
0.0002
5.3
7.6
5.9
3.0
0.0
0.0
0.0
BENEFITS
1988
$20,639 •
$29,725
$23,023
$11,616
$0
$0
$0
POP
7371
9828
9167
8505
7844
7182
6521
BENEFITS
1989
$20,956
$30,012
$23,167
$11,642
$0
$0
$0
POP
7466
9960
9223
3514
7796
7088
6379
BENEFITS
1990
$21,227
$30,415
$23,308
$11,655
$0
$0
$0
POP
7475
9970
9308
8647
7985
7308
6653
BENEFITS
1991
$21,252
$30,445
$23,523
$11,337
$0
$0
$0
POP
7484
9979
9356
3757
8146
7529
6930
BENEFITS
1992
$21,278
$30,473
$23,644
$11,987
$0
$0
	 $0
21.3    $85,053
                              $85,778
                     $86,605
                   187,058
 587,383
37,0   $339,492
$342,210
$345,29
                                                                   $347,'
    ,359

-------

-------
  probablility  that  a blood lead level  will fall below the CDC
  blood  lead  level  criteria for  lead poisoning.
      Secondly,  the methodology employed  in this analysis
  implicitly  assumes that  water  lead and blood lead are independent
 of each other.  This  ignores the  fact that higher blood lead
  levels are  the  result of  greater  exposure to lead,  and  probably,
 people who  have higher blood lead  levels  are more likely to have
 higher lead lead levels in their  drinking  water.   A more
 realistic methodology would produce a higher probability that  a
 child falls below 25 pg/dl because it would  assign  the  larqer
 reductions in  lead exposure from drinking  water to  high  lead
 children  when  simulating the new blood lead  distribution.   Under
 the independence assumption,  however,  high lead individuals  face
 the same  reductions as low lead individuals, reducing the
 probablity of  falling below 25  pg  and  biasing down th*> benefit
 estimates.
      Finally,  and  most importantly, the  monetary estimate
 comprises  only avodied medical  costs associated with the
 treatment  of lead  poisoning and avoided expenses for compensatory
 education.   A  number  of benefit categories have been excluded
 from the analysis because  the relationship between blood lead
 levels and certain  health  effects  have yet  to be precisely
 specified.   Such benefits  include  avoided  costs associated with
renal damage,  a  very serious effect of lead exposure,  increased
risk of anemia,  vitamin D  deficiency, and  permanent  nerve damage.
The analysis also includes  benefits that are  exceeding difficult
to quantify such  as avoided pain and suffering  associated with

-------
medical care and reduced quality of  life resulting  from  the

permanent effects of damaged cognitive development.



HEALTH BENEFITS  	 ADULT WHITE  MALES.  AGES  4O-59
     Although the public health community  has  long  known  about

the link between high lead exposure  and  elevated  blood  pressure,

it is only recently that research has  uncovered  effects at  low

levels of exposure.  Prior to the analysis of  the MHANES  II  data

by CDC- and EPA personnel, a number of  investigations reported a

statistically significant relationship between low to moderate

blood lead 1'evels and blood pressure in  males.   In addition  to

epidemiological analyses, animal studies also  demonstrate this

link.'*''  The research also indicates possible  causal pathways by

which lead acts oh the cardiovascular  system.   ""Iiese include

renal changes and inhibited uptake of  calcium,  an element which

suppresses blood pressure.  Besides  demonstrating a strong  and

significant relationship between blood lead levels and  blood

pressure, the analysis of the NHANES II  data showed that  there

was no threshold level of exposure.  In  other  words, there are

blood pressure effects at any blood  lead level down to zero.***

     Because of lead's direct contribution to  hypertension,  the

toxin is also associated with cardiovascular disease CCVD)

resulting from elevated blood pressure.  Two extensive studies,
47 U.S. EPA, Costs  and  Benefits of  Reducing Lead in Gasoline.
pp.V-4 - V-5.

48 Ibid.. pp.V-S -  V-15.

-------
                                  27



  the Framingham and the Pooling  Project,  have assessed the  risk  of


  CVD (strokes,  myocardial infarctions,  and deaths resulting  from


  all  forms  of CVD) based on several  important variables, including


  blood  pressure,  serum cholesterol,  and smoking.   The


  corresponding  risk regression equations  show a very strong


  relationship between CVD and blood  pressure. •»»  Since blood


  pressure seems to increase with blood  lead,  so. too will  the


  incidence  of CVD.


      To calculate reduced cases of  hypertension  and' incidence of


 CVD, we must determine the impact of lower lead  exposure from


 drinking water on  blood  lead  levels in adult  men.   While a number


 of epidemiological  studies  have been performed which  relate water


 lead to blood  lead  in  adults,  the Pocock study is  perhaps  the


 best.  His study  is especially relevent to this  analysis because


 i.t measures effects at lower  water lead concentrations.  His


 findings are summarized in  the following equation:


                             PbB = a •+• .OSPbW
      where:

           PbB = blood  lead  in  jjg/dl

           a   = constant plus  other  demographic and
                 environmental  factors,  and
           PbW = water  lead  in  yg/L (standing  grab smaple).


 Using this  regression equation and the  estimate of reduction  in


 water lead  levels, the mean reduction in  blood lead is estimated


 to be 1.33  pg/dl  (. OS * 22.2 jjg/L) .  Accounting for changes in


 gasoline lead,  blood lead  for  the  average  male will decline from


 3.25 pg/dl  to 6.92 jjg/dl  in 1988.
49 Ibid.f  pp.V-29  -  V-31.

-------
                               23
Hypertension








     Medical authorities consider  adults having diastolic blood




pressure greater than 9O to  be  hypertensiy*-   Elevated blood




pressure dramatically increases the risk of all forms of cardio-




vascular disease and thus  requires medical  attention.  Treatment




costs for hypertension  include  visits to a  physician, medication,




hospital stays, and the opportunity costs of lost working days,




and when combined, total $250 per  year.150



     While, calculating the  reduction in cases of hypertension




for adult males employs on a fairly direct  method, the process  in




this analysis  is complicated by that fact that the logistic




regression  developed by Pirkle  and Schwartz C1385), which




estimates the  probability  that  an  adult male will be



hypertensive,  performs  poorly at b1 :-od lead levels <10 pg/dl .




Consequently,  this analysis does not make a quantitative




estimate.   While  it  is  likely that there will  be  a reduction  in




cases of hypertension,  the number  will be small and  the  omission




will not seriously affect  the outcome of the analysis.   It  is,




however, one  of  the factors which contribute to a conservative



estimate of the  benefits.
 Cardiovascular  Disease







      Having previously  estimated  the reduction in blood lead



 resulting  from  reduced  lead  levels in drinking water, calculating





 SO  Ibid..  p.  V-38.

-------
                                 23






 the  reduced  incidence of CVD requires that we first estimate the




 change  in  blood  pressure,  and second, estimate the change in risk



 of suffering  from  various  forms of CVD.




      By using the  before and after blood lead values Ci.e.




 8.25 pg/dl and 6.92 pg/dl)  in the NHANES II regression equation




 linking blood lead and blood pressure,  we calculated the change.




 in blood pressure.  We then  used  the  before and  after  blood




 pressure values  in the CVD  risk regression equations in order to




 estimate the change in probability that  an individual  will suffer




 from CVD.   By applying the changes in probability to the adult




 white male population, we were able to estimate  the avoided



 incidence of CVD.CSee table  III)
 Myocardial  Infarction*.  In this analysis, the  benefit  estimate




 for  Myocardial  Infarctions (Mis!) is based on an EPA  calculation




 that  includes medical  costs Cbuth physician and hospital)  as  well




 as  lost  wages.»»   Although fatal Mis are included, the  benefits




 measure  in  this category does not account for the value of  a  lost



 life.  This valuation  is treated in a later section.




      The  estimate  of avoided  Mis is based on the Pooling




 Project's risk  assessment  in  which  the probability of suffering a




 MI was calculated  as a  function  of  age,  smoking behavior, serum




cholesterol,  And diastolic  blood pressure.   We derived  the  change




 in the probability of suffering  an  MI  from the change in blood




pressure.   Multiplying  the  probability differential  by  the




population  yields the estimate that  2.95 Mis  can be  avoided in



51 Ibid.. p. V-33.

-------
PARAMETERS
serum cholesterol
average age
'..^feline blood pb
Blood pb reduction
percent applicable
                                           TABLE III
                                         ADULT BENEFITS
 213
  50
17.4
1.33
  547.
                                  AVOIDED MYQCARDIAL INFARCTIONS
PARAMETERS
avoided cost per MI
smoking
       start blood lead-
       end blood lead
       start blood pressure
       end blood pressure
       start profa MI
       end prob MI
       Di f prob MI
       population
       avoided Mis
       benefits
$£5,600
0.8
1988
8.25
6.92
81.53
80.72
0.00658
0.00643
0.00015
36100
2.95
$193,410
1989
8.23
6.90
81.51
30.70
0.00658
0.00643
0.00015
36800
3.01
$197,728
1990
8.22
6.89
81.51
80.70
0.00658
0.00643
0.00015
37500
3.07
$201,682
1991
8.20
6.37
81.50
30.68
0.00658
0.00642
0.00015
33800
3.19
$209,074
1992
8.19
6.86
81.49
80.68
0.00657
0.00642
0.00015
40250
3.31
$217,096
                                         AVOIDED STROKES
PARAMETERS
avoided cost per stroke
smoking
       start blood  lead
       end blood  lead
       itart blood  pressure
       end blood  pressure
       starb prob s-trok*
       end prob  stroke ,
       Di f prob stroke
       population
       avoided strokes
       benefits
        $49,000
           8.12
                                        1988
                             1989
1990
                                                                         1991
1992
8.25
6.92
125.66
124.16
0 . 00347
0 . 00333
0.00009
36100
1.75
$114,642
3.23
6.90
125.63
124. 13
0.00347
0 . 00333
0 . 00009
36300
1.79
$117,194
3.22
6.39
125.63
124.12
0.00347
0 . 00333
0 . 00009
37500
1.32
$119,534
8.20
6.37
125.61
124.10
0 . 00347
0 . 00338
0 . 00009
33800
1.89
$123,910
3.19
5.36
125.60
124.09
0 . 00347
0.00337
0 . 00009
40250
1.96
$128,661

-------
                                        TABLE 11 Hie out.)
                                         AVOIDED DEATHS
PARAMETERS
avoided cost per death     $1,000,000
smoking                          2.24
       start blood lead
       end blood lead
       stare blood pressure
       end blood pressure
       starb prob death
       end prob death
       Dif prob death
       population  -
       avoided Mis
       benefits

       TOTAL CVD
198S
3.25
5.92
Q H CT-~.
Ola ^JO
80.72
0.01314
0.01282
0.00032
3S100
6.28
$6,278,513
1989
8.23
S.90
81.51
80.70
0.01314
0.01231
0.00032
36300
6.42
$6,418,852
1990
8.22
6.39
31.51
30.70
0.01314
0.01281
0.00032
37500
6.55
$6,547,245
1991
8.20
6.37
81.50
30.63
0.01313
0.01281
0.00032
33800
6.79
$6,787,263
19'11'"
3. 19
6.35
31.49
30.68
0.01313
0.01231
0 . 00032
40250
7.05
$7,047,689
-r-*fTf * «• r J «*••*»* f9J V^* • \J\J _f


$7,120,247 $7,393,446

-------
                               30






1988, increasing to 3.3 in  1992.   In  monetary terms,  we valued an




MI at $65,SCO, yielding total annual  benefits avoided Mis at




$193,000 in 1988, rising to $217,000  in  1992.S:3S








Strokes.  Strokes are a debilitating  form of cardio-vascular




disease that can leave parts  of  the central  nervous system



permanently damaged.  In estimating the  benefits achieved from




avoided strokes, the analysis includes only  medical costs and




foregone wages.



     The estimation procedure uses the Fr am in gharri study risk




reqression equation assessing the  probability of suffering a




stroke based on  systolic blood  pressure, age, smoking behavior




and  merum cholesterol.a3   Using  the same procedure employed  for




Mis, we estimated that  1.75 strokes can be avoided, rising to




1.96 in 1992;  at $49,OOO per  stroke,  this produces  benefits of




$115,000  o.n 1988 and $129,000 in 1992.=*
Deaths.   In  addition  to assessing risks for strokes, the



Frarningham study  estimated risk regression equations for deaths




as a  function  of  diastolic blood pressure, smoking, and




cholesterol.   The study looked at death from all causes




associated with blood pressure, not only myocardial infarctions




and strokes. s=s
52  Ibid..  p.  V-3S - V-39.




53  Ibid.,  p.  V-31.




54  Ibid..  p.V-40.




55  Ibid..  p.  V-31.

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                                *3 1
                                vi 1






     Again  using  the blood pressure calculations  from  above,  we




substituted the blood pressure values into the risk  regression




equation  to calculate the change in -probabi-1 ity.  We then  applied




the probability differential to the Boston population  to estimate




the reduction  in  expected deaths.   This processs  yields the




estimate  that  6.3 deaths can be avoided by reducing  water  lead




levels  through additional corrosion treatment, a  figure that




rises to  7  in  1992.




     Monetizing the  benefit  of saving lives has alwa'ys been




controversial.  We used  the  somewhat conservative estimate that




saving  a  statistical  life is worth a million dollars.  Thus,  the




benefits  in  terms of  lives saved in 1988 is $6,300,COO,




increasing  to  $7,OOO,OOO in  1992.









Total Benefits for Adult Males
          Having  calculated  the avoided myocardial infarctions,




strokes, and deaths,  I  estimate the total benefit for this




age/sex group of  the  population to be *6,60O,OOO in  1988 and



7,400,000 in 1992.




     There are several  substantive issues,  though, that suggest




that this benefit measure  is somewhat conservative.   First, we




have excluded 'non-black  men  outside the 40—59 age group and as




well as blacks of all age  groups.   Blacks were excluded because




the Frarfiingham and Pooling Project studies did not have a




sufficiently large sample  to develop risk assessments.  With




respect to the age issue,  it is difficult to seperate the effect;

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of aqe and blood pressure outside  this  age group.   It is likely,




however, that exposure to lead  will  increase the incidence of CVD




in these other population groups.



     Secondly, the analysis  excludes other kinds of health




effects of lead exposure such as renal  damage.   These effects




have not been included because  medical  and epidemiological



research has yet to determine precisely the relationship between




blood lead and extent of physiological  damage.   While renal




problems can often be treated,  medical  care is  very expensive and




often accompanied by adverse emotional  impacts.   In addition,




renal damage affects all age and sex groups.  It is therefore a




very important omission from the benefits calculation.




     Thirdly, the cardiovascular monetized estimate fails to




consider quality of life issues.   The benefits  of avoided




myocardial infarctions and strokes included only medical costs




and lost wages.  They fail to account for the kind of limits




placed on the lives of heart attack  survivors.   Stroke victims




who may suffer from partial  paralysis and loss  of speech




facilities dramatically diminish the quality of  life.




     On the other hand, the  analytic methodology used to estimate




CVD related benefits may lead to an  upwardly biased measure.  The




first bias results from the  use of national blood lead data  for




adult men.  Because adult males in Boston probably have higher




blood lead levels than their counterparts in the national sample,




the mean blood lead level used  here is  probably low.  Since  the




relationship between blood lead and  CVD is log  linear, an




equivalent reduction in blood lead will have a  larger impact on

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 CVD  when  using a lower mean blood lead level.  Therefore,  an




 upward  bias  has been introduced.  Sensitivity analysis, however,




 indicates that this bias is relatively small.




     A  second  bias arose from the way we calculated blood




 pressure  changes.   When using the regression equations to




 estimate  blood pressure,  we sustituted the mean values for all



 the  variables.   In order  for such a procedure to produce unbiased




 reuslts,  there would have to be no correlation between the




 independent  variables.   Since correlations probably -do exist,  the




 results are  biased.   Without knowing the correlations, though,  it




 is impossible  to determine the direction of bias.




     In the  absence of good health data specifically  for Boston,




 simplifications are necessary in order to perform the analysis.




 The  problem  of  bias,  however,  is relatively small and




 overwhelmingly outweighed by both the health effects and




population groups  excluded from the analysis.  Nevertheless, we




 will perform sensitivity  analysis in a later section to




compensate for  various weaknesses and test the strength of the



 result s.








MATERIALS BENEFITS
     In addition to  lower  lead  concentrations in drinking water




and its associated health  benefits,  additional  treatment of




corrosive water will  further  reduce  materials damage.  This




benefits category is  important  when  we consider the enormous




investment in capital plant associated with water supply.  Aside

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                                34


 from the petrochemical  and  electric power supply industries, the

water supply and  wastewater treatment industry represents the

 largest value  in  capital  plant.   Corrosion damage is particularly

acute in consumer  systems where water velocity has high

variability, pipes are  smaller,  and temperatures are higher, all

characteristics which increase corrosion rates.  Consumer systems

also experience galvanic  corrosion associated with the

combination of lead  sol'der  and copper pipes.   Because of the

large capital  invsetment, enormous savings can be achieved  from

extending the  life of pipes and  other components such as hot

water heaters  and  air conditioning systems.

     Because' corrosion  damage  has not been examined in Boston,

this analysis  relies heavily on  a study of Seattle performed by

Kennedy Engineers  in the  late  1970s.   Using  this study is

appropriate because  Seattle and  Boston have  very corrosive  water

supplies.  We  are  also  hampered  by the lack  of direct measures of

corrosion rates for  Boston.  Consequently, the analysis uses lead

concentrations as  a  proxy.

          In 1978,  Kennedy  Engineers  estimated annual corrosion

costs to be $7,400,000: $7,000,000 for consumers and $400,000 for

the water utility  or $22. SB/capita in 1985 dollars.*5*

Furthermore, the National Bureau of Standards believed that

corrosion control  techniques used in  the 1970s could reduce the

costs of materials damage by 207..   Based on  this Judgement,  the

avoidable per  capita cost is $4.53.
56 Ryder, Journal of the American  Water  Works Association,  May
198O, p.283.

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                                 35


      To calculate the additional  damage costs avoided by  using

 the treatment discussed  in  this paper,  it is necessary  to

 estimate the incremental reduction in corrosion. Using  the  Region

 I lead concentration data as  a  proxy, I estimate that an

 additional 25% reduction in corrosion will  be achieved.8"'

 Applying this incremental improvement to the savings already

 achieved,   we can expect an additional  $1.13/capita reduction in

 materials  damage annually from  the new  treatment or $635,000  for

 thecity.  •

      Benefits can also be derived  in  a  second way.   This  method

 utilises the conclusions reached by the AWWA concerning corrosion

 control  and  avoidable costs.  According to  the AWWA, the

 effectiveness of corrosion control  ranges from 30%  to 90%, while

 the corrosion costs may be reduced  by 157. to 50%.=«»  Usinq the

 Region  I data and assuming the  prescribed treatrnenb will maximize

 corrosion  control,  the 'effectiveness  of control  will increase

 from  757. to  'BO'/..   Assuming a linear relationship between

 corrosion  control and reduced materials damage,  this 15%

 improvement  in  control  will  result  in a 9.757. reduction  in

 materials  damage or  $2.21/capita annually C. 0975 *  $22.68!!.

 Total cost reduction in  Boston would  therefore be $1,242,000.

 averaging  the two estimates  we arrive at  a  benefit  figure of

$939,000 annually for  reduced materials  damage.
By
57 Karalekas,  "Control  of Lead,  Copper, and  Iron  Pipe Corrosion
in Boston", p. 93.   NaOH treatment reduced the mean  standing grab
lead concentration  by .087 rng/L.  Additional  treatment will
probably reduce the concentration by another  .022 rnq/L which
represents an  additional  25% improvement.

38 AWWA, op.c j t. . p.  590.

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                                ^c
                                oo
RESULTS  AND  DISCUSSION



     To complete  the analysis,  we aggregated the costs and

benefits  and  compared them  to derive the net benefit.  We also

performed  some sensitivity  analysis to test the strength of the

results and to compensate  for some of the uncertainties arising

from the  data  and the analysis.  Finally, we considered how

representative these results are for the nation as a whole.

     On the treatment side,  based on the judgment that the MWRA

will employ additional  pH adjustment and will add zinc

orthophosphate, the  utility will incur total costs of

approximately  $1,600,000.   Because all MWRA consumers would reap

the benefits  of additional  treatment, it is reasonable to

apportion  costs to Boston based  on its consumption. =l'*  According

to bhe MWRA demand projections,  Boston consumes 437. of the

region's  water.*"0 Therefore, Boston's share of the treatment

costs based on consumption,  would be $700,000.   The utilization

of less expensive methods could  dramatically lower this figure.

For example,  if additional  pH adjustment alone was sufficient,

the costs  for  Boston would  be only *45,OOO.
59 Suburban residents  would  certainly see a reduction in
materials damage.  On  the  health  side,  benefits would probably be
smaller.  Lead materials,  however,  are found in other member
communities so that additional  treatment  would lower lead
concentrations in these  other  communities.

£0 Metropolitan District Commission,  Water  demand projections.
Prepared by Wallace, Floyd,  Associates Inc.,  January 1983, p. IS.

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                                 37






      With respect  bo  benefits,  the analysis has examined  three




 major categories:  avoided  neurological damage in children,




 reduced CVD in adult  white  men  aged 40-59 ,and reduced materials




 damage.  When added together, these benefits for Boston are




 $7,300,000 in 1988 increasing to *8,70O,OOO in 1992  Csee  table




 IV).   When the aggregate costs  and benefits are compared, this



 analysis indicates that additional corrosion control in Boston




 will  produce a positive net benefit of  $7,20O,OOO in 198S,




 increasing to $8,000,000 in 1992.   In  terms of benefit/cost




 ratios, the result are 11.5:1 increasing to 12.7:1.




      Because much of the work on  the relationship between CVD  and




 lead  has yet to be replicated in  other  analyses ,  we should also




 consider the benefits excluding  that category entirely in which




 case  benefits are *1,30O,OOO in  1988, a value which  increases




 slightly over  the five year period.  Excluding  the CVD benefits,




 the analysis still yields a positive annual  net  benefit of



 *SOO,OOO in  1988.




      Since our  calculations involve a number  of  staqes Ci.e.




 estimating  water  lead  reduction, linking water  lead  to blood




 lead, etc)  and  uncertainities at each stage,  an  exhaustive




 sensitivity  analysis  could  generate a huge number  o-f  possible




 outcomes.   To simplify matters we developed only two  alternate




 cases:  the pessimistic case  with highest costs and lowest




 benefits and the  optimistic  case with lowest costs and  hiqhest



b en e f i t s.




           For our  optimistic  alternative, we used the  AWWA




treatment cost estimate,  Driven by lower chemical costs,

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                                     TABLE IV
                                  TOTAL  BENEFITS
children
myocardial infarctions
strokes
deaths
materials damage	
                                 1988
                 1989
1990
                                                                  1991
  $339,492   $342,210   $345,292   $347,351   3348,359
  $193,410   $197,723   $201,682   $209,074   $217,096
  $114,642   $117,194   $119,534   $123,910   $128,661
$6,273,613 $6,418,852 $6,547,245 $6,787,263 $7,047,689
  $939.000   $939fOOP   $939.000   $939.000   $939.000
total w/o CVD

total
$1,278,492 $1,281,210 $1,284,292 $1,286,351 $1,287,859

$7,865,157 $8,014,983 $8,152,753 $8,406,599 $8,631,305

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                                     TABLE V
                             COST BENEFIT CQMPARISION
net total
b/c ratio

net w/o CVD
b/c ratio w/o CVD
                                 1988
                 1989
1990
1991
19-32
$7,179,176 $7,329,003 $7,466,773 $7,720,818 $7,995,324
      11.5       11.7       11.9       12.3       12.7

  $592,511   $595,229   $598,311   $600,371   $601,678
       1.9        1.9        1.9        1.9        1.9

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                               38






Boston's share of annual treatment cost would be $550,000.   To



calculate benefits we used the following assumptions:  apply  water



lead data to 707. of the population; use the high 357.  confidence



interval for water lead reduction - .026 mg/L;  and  the high



estimate for materials damage - $1,242,000.  Under  these



assumptions we calculated annual benefits  to be $11,500,000  for



Boston in 1989, rising to $12,775,OOO  in 1992 Csee  table  VI).



     In the pessimistic case, we based treatment cost  estimates



on EPA's high phosphate feed rate assumption.   Boston's share of



the region's annual cost would be $860,000.  On the benefits



side, we employed the following assumptions to  develop the  low



estimate: apply water lead data applies to only 40% of the



population;  use the low 957. confidence interval for water lead



reduction - . O18 rng/L; and the low estimate for materials damage



- $635,000.   This scenario yielded $3,350,000 in annual net



benefits for Boston in 1988, rising to $4,330,000  in  1992 Csee




table VII).



     Even under pessimistic assumptions, the Boston case  study



clearly confirms the  findings of EPA's earlier  studies of the



whole country:  in terms of health and materials benefits,



corrosion control is  a worthwhile investment.   What is even  more



impressive about these results is the  fact that they  represent



the marginal effects.  Like many pollution control  activities,



corrosion control is  often characterized by decreasing marginal



benefits.  This implies that the benefit per dollar of treatment



declines as additional treatment is implemented.   Therefore, in



Boston, a city that already controls corrosion  somewhat,  the

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                                         TABLE VI
                                     TOTAL BENEFITS
chi idren
myocardial
•strokes
deaths
mat trials
            infarctions
                                 1988
                                             1989
                                                         1990
                                                                     1991
                                                                                 199;
total
   4495,375     $499,544     $504,264     5507,002     $509,003
   $302,508     $309,279     $315,470     $327,045     $339',599
   $179,239     $183,238     $136,901     $193,749     '5201,181
  $9,320,761  $ 10,040,666  $ 10, 241,590'  $ 10,617, 533  $ 11,025, 128
  $1.242.OOP  $1.242.OOP  $1.242.OOP  $1,242,OOP  $1.242.000
                           $12,039,883 $12,274,726  $12,490,325  $12,887,329 $13,316,911
                               COST BENEFIT COMPARISON
                                 1988
                                            1989
                                                         1990
                                                                    1991
                                                                                 1992
net
b/c
    total
    ratio
$11,499,366 $11,734,709 $11,950,303 $12,347,312 $12,776,393
       17-£        17.9        18.2        13.3         19.4

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                                       TABLE VI!
                                    TOTAL BENEFITS
children
myocardial infarctions
strokes
deaths
materials damage   	
                                            1939
                            1990
            1991
1992
total
  $180,096    $181,639    $183,401    $184,343    $185,021
  $114,594    $117,146    $119,487    $123,862    $123,512
   $67,951     $69,459     $70,346     $73,436     $76,251
$3,719,837  $3,302,728  $3,373,725  $4,020,773  $4,174,982
  $635.000    $635.000    $635.000    $635^000    $635.000

$4,717,477  $4,805,973  $4,887,459  $5,037,419  $5,199,856
                               COST BENEFIT CQMPARI5IDN
                                1988
                1989
1990
1992
net total
b/c ratio
$3,848,092  $3,936,587  $4,018,073  $4,168,034  $4,330,480
       6.9         7.0         7.1         7.3         7.6

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 marginal benefits generated  by  additional  treatment will be much




 lower than the marginal  benefit  for  communities that do not




 currently treat their water.  On  the other hand,  health benefits




 are more pronounced because  the presence of lead  in the water




 distribution system is more  widespread  in  Boston  than in many



 other communities.




      The discussion of marginal benefits,  though  does raise one




 problem not adequately addressed  in  this paper.   While this




 analysis has examined the combined benefits of  additional  and




 better  controlled pH adjustment and  zinc orthophosphate,  it was




 not  possible to isolate the incremental benefits  produced  by each




 treatment  alone.   We are therefore left with the  small




 possibility that  the vast proportion of lead reduction  results




 from the relatively  inexpensive pH adjustment, while  very  Tittle




 results  from  the  relatively expensive orthophosphate  treatment.



 Consequently,  we  car. conceive of instances  where large




 additional  investments in treatment are required to meet the




 contemplated  MCL  but are  not  warranted in terms of the health and




 materials benefits they  yield.   In such instances, EPA should




 consider granting a  waiver.   Otherwise,  inflexible enforcement of




 the  MCL  may force water utilities  to  invest additional resources




 to treat corrosion related  contamination when such resources




 could be directed at other  problems to yield greater water



quality benefits.

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                                4O
RECOMMENDATIONS
     My analysis shows that EPA  should  lower  the MCL for lead




from .05 mg/1 to .01 mg/1 .  The  measures  necessary to accomplish




this task are relatively  inexpensive  and  the  technologies are




simple.  The potential benefits  are large and extend beyond the



health effects of lead exposure.   Corrosion control  will lower




the level of other toxic  and nuisance contaminants and reduce




materials damage.



     Along wi'th the change in  the  MCL,  EPA should consider




instituting a waiver system.   While all communities that have




corrosion related lead contamination  of their drinking water




should undertake corrosion control  bo reduce  lead concentrations,




EPA should be sensitive to mariginal  costs and benefits, and




adopt a secondary standard of  perhaps .015 mg/L.  If a community




achieves this standard and can demonstrate that additional




improvements would not be warranted in  terms  of breatrnent costs,




a waiver from the .01 mg/L standard might be  indicated.   The




latter requirement will be increasingly difficult to meet,




though, as additional health effects  of lead  are better




understood and monetized  (i.e. renal  damage)   Consequently,




waivers would only be granted  in cases  where  a community just




barely exceeds the MCL and further reductions in lead would




require significant new investments in  corrosion control.




     Finally, EPA, through its regional offices, should  provide




technical assistance to cities and municipalities.  Before a




community chooses an appropriate treatment method it must first

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                                41






analyse its supply water  and  survey th« types and extent of




materials  found in its distribution system.     Communities must




also institute a comprehensive  monitoring  plan in order  to




evaluate the effectiveness of the corrosion  control  and  to make




changes as needed.  EPA should  assist utilities  with  the




necessary studies and help them develop treatment  strategies.
                           •frU. S.GOVERNMENT PRINTING OFFICE I 1988-516-002/801 50

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