O?30omo 19
REDUCING LEAD IN DRINKING WATER:
A BENEFIT ANALYSIS
Ronnie Levin
Office of Policy, Planning and Evaluation
U.S. Environmental Protection Agency
1PA-230-09-86-019
Draft Pinal Report
December 1986
(revised Spring 1987)
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ACKNOWLEDGEMENTS
Many people contributed to the publication of this documents
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
CHAPTER I: INTRODUCTION
I.A. BACKGROUND !MFOEMATION
I.E. SUMMARY" OF REPORT
LB 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
CHAPTER II; OCCURRENCE OF LEAD IN DRINKING WATER
II .A. SOURCES OF LEAD IN DRINKING WATER
II.A. 1. Variables Affecting Lead Levels in Drinking Water
II.A.l.a. Key Water Parameters Affecting the Solubility of Lead
II.A.l.b. Lead Solder
II.A.l.c. -Lead Pipes
II.A.l.d. Other Potential Sources of Lead
II.A.I.e. Other Factors Relating to Lead Contamination Levels
II.A.l.f. Summary
II.A.2. Prevalence of Lead Materials in Distribution Systems
PAGE
1-1
1-2
1-5
1-10
1-16
1-19
1-22
I-25
II-2
II-3
11-4
11-6
11-10
11-10
11-12
11-13
11-14
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Table of Contents
PAGE
II.B. mm OS THE OCCURRENCE OF LEAD IN DRINKING WATER 11-16
II.B.l. Patterson Study/Culligan Data on Tap Water 11-18
II.B.i.a. Consistency with Other E&ta 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 II-41
II.C.l. 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. Estirrate of Exposure to Lead in Drinking Water
to Inhabitants of New I^ousing 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 CHIIDREN'S EXPOSURE TO LEAD
III.A. PATHOPHYSIOLOGICAL EFFECTS III-6
III.A.l. Effects of Lead on Pyrlmidine Metabolism III-ll
III .A. 2. Effects on Heme Synthesis and Related
Hematological Processes III-ll
III.A.2.a. Mitochondrial Effects 111-12
III .A.2.b. Heme Synthesis Effects 111-12
III.A.3. Lead's Interference with Vitamin D Metabolism
and Associated Physiological Processes 111-13
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Table of Contents
EAGE
III.A.4. Stature Effects
III .A.4.a. Effects of Lead on Fetal Growth
III.A.4.b. Effects of Lead on Pest-Natal Growth
III.A.4.c. Sumtary of Stature Effects
III.B. NEUROTOXIC EFFECTS OF LEAD EXPOSURE
III.B.l. Neurotoxicity at Elevated Blood-Lead Levels
III.B.2. Neurotoxicity at Lower Blood-Lead Lewis
III.B.2.a. Cognitive Effects of lower Blood-Lead Levels
III.B.3. The Magnitude of Lead's Inpact on IQ
III.C. FETAL EFFECTS
III.C.l. Assessing the Benefits of Reduced
Fetal Exposure to Lead
III.D. MONETIZED ESTIMATES OF CHILDREN'S HEALTH BENEFITS
III.D.l. 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
III.E. VALUING HEfiLTH EFFECTS: CAVEATS AND LIMITATIONS
III.F. SUMMARY OF ANNUAL MONETIZED AND NON-MONETIZED
CHILDREN'S HEMLiTH BENEFITS
111-17
111-18
I11-20
111-26
111-28
TXT OQ
Xxi."BAO
111-31
111-34
III-40
111-42
111-44
111-49
111-50
111-54
111-55
II1-56
II1-60
III—62
II1-67
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Table of Contents
PAGE
CHAPTER IV: HEALTH BENEFITS OF REDUCING LEAD: ADCJLT ILLNESSES
IV.A. THE RELATIONSHIP BETWEEN BLOOD LEAD LEVELS AND BLOOD PRESSURE IV-2
IV. A. 1. Epidemiological Studies of Blood Lead Levels IV-3
and Hypertension
IV.A.1.a. Occupational Studies IV-4
IV.A.l.b. Observational Studies IV-5
IV.A.I.e. Population Studies IV-7
IV.A. 2. Mectianisms 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-3 5
IV.A.4.b. Myocardial Infarctions, Strokes, and Deaths IV-35
IV.B. LEAD'S EE-EECTS UPON REPRODUCTIVE EUNCTION IV-40
IV.B.l Estimating the Population At-Risk for
Female Reproductive Effects lV-^43
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Table of Contents
PAGE
IV. C, MONETIZED ESTIMATES OF ADULT HEALTH BENEFITS!
REDUCED CARDIOVASOJIAR DISEASE RISK IN MEN IV-45
IV.C.l. Hypertension IV-46
IV.C.2. l^ocardial Infarctions IV-47
IV.C.3. Strokes IV-51
IV.C.4. Mortality IV-53
IV.C. 5. Sumrrary of Annual Monetized Benefits
of Reduced Cardiovascular Disease IV-54
IV.D. VALUING HEALTH EFFECTS: CAVEATS AND LIMITATIONS IV-56
IV.E. SUMMARY CF ANNUAL MONETIZED AND NONMDNETIZED ADULT HEALTH
BENEFITS OF REDUCING EXPOSURE TO LEAD IN DRINKING WATER IV-60
CHAPTER V: BENEFITS FROM REDUCED MATERIALS DAMAGE
V.A. THE CHARACTERISTICS OF AGGRESSIVE WATER V-4
V.A.I. Parameters of Water Affecting Corrosivity V-5
V.A. 2. The Electrochemistry of Corrosivity V-8
V.A.3. Types of Corrosion V-9
V.A. 4. Corrosion Indices V-10
V.A.5. PluntxDsolvency and Other Factors
Determining Lead Levels in Drinking Water V-12
V.B. DAMAGE TO PUBLIC SYSTEMS FROM INTERNAL OORROSION V-15
/
V.B.I. Occurrence of Corrosive Water in the United States V-15
V.B.2. Corrosion Damage V-20
V.B.3. Estimating the Annual Costs of Corrosive Water V-22
V.B.4. Monetized Benefits of Reduced Corrosion Damage V-29
BIBLIOGRAPHY"
APPENDIX As BOSTON CASE STODY
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LIST OF TABLES
CHAPTER I;
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
1-21
TABLE 1-3 Summary of Estimated Annual Monetized
Benefits of Reducing Exposure to Lead
from 50 ug/l to 20 ug/l (1985 dollars)
for Sample Year 1988
1-23
TABLE 1-4 Surrmary of Estimated Annual Non-Monetized
Benefits of Reducing Exposure to Lead from
50 ug/l to 20 ug/l for Sample Year 1988
1-24
CHAPTER lis
TABLE 11-1
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 toy
Age of Plumbing (Field Studies)
11-39
TABLE I1-4
Percentages of Samples Exceeding 20 ug/l
of Lead at Different pH Levels, by Age
of House
11-44
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LIST OF TABLES
CHAPTER III:
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 Sairple 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
II1-68
CHAPTER IV:
TABLE IV-1 Benefits of Reducing Strokes
IV-52
TABLE IV-2
Summary of Annual Monetized Blood-
Pressure Related Benefits of Lcwered
MCL for Sample Year 1988
IV-55
TABLE IV-3
Surrmary 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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LIST OF FIGURES
CHAPTER III:
PAGE
FIGURE III-l Multi-Organ Impacts of lead's Effects
on the Heme Pool
III-2
FIGURE III-2 Surrmary 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 W-l Adjusted Rates of Death and Heart Attadcs W-37
versus Blood Pressures Erandngham Data
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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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 MCLGj 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.B. 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.
Ethylene dibrcmide
2.
Alachlor
14.
Heptachlor and Heptachlor
3.
Aldicarb, Aldicarb sulfoxide and
epoxide
Aldicarb sulfone
15.
Lindane
4.
Carbofuran
16.
Methoxychlor
5.
Chlordane
17.
Monochlorobenzene
6.
Dibrcmochloropropane
18.
Polychlorinated biphenyls
7.
o- ,m-Dichlorobenzene
19.
Pentachlorophenol
8.
cis- and trans-1,2 Dichloroethylenes
20.
Styrene
9.
1,2-Dichloropropane
21.
Toluene
10.
2,4-D
22.
Toxaphene
11.
Epichlorohydrin
23.
2,4,5-TP
12.
Ethylbenzene
24.
Xylene
B. Inorganic Chemicals
1. Arsenic
2. Asbestos
3. Barium
4. Cadmium
5. Chromium
6. Copper
7. Lead
8. Mercury
9. Nitrate aid Nitrite
10. Selenium
C. Microbiological ?arameters
1. Total Coliform Bacteria
2. Turbidity
3. Giardia
4. Pathogenic Viruses
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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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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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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 distribution
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 EPA1s 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
Abstract of the 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
° 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);***
° 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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° because the Culligan data represent water that is
harder than average, whereas high lead levels are
often found with soft waters; and
° 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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(for children)^ 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.B.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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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
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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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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 (6-20 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.B.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
_in 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
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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
effects are discussed above, under children's 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.B.4. Benefits of Reduced Materials Damage
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 t'rve most part, therefore, treatment
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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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1-21
TABLE 1-2. Estimates of Annual Per Capita Corrosion Damage (1985 dollars)
Corrosion
Studies
Estimated Annual Corrosion Damage
(per capita)
Damage
Avoidable
Through
Water
Treatment
Annual Per
Capita Benefits
of Corrosion
Control
Assumptions/Notes
Distribution
Systems
Residential
Total
Kennedy Engineers
(1973)
$5.57
—
$16.71*
30%*
$5.01*
Assumed 30% potential reduction
in corrosion damage and that dis-
tribution costs were one-third o:
total costs.
Hudson & Gilcreas
(1976)
$8.68*
$26.04*
50%
$13.02*
They did not include increased
operating costs. Per capita
estimate assumes 200 million
people are served by public watc
systems. Assumed that distri-
bution costs were one-third of
total costs.
Kennedy Engineers
(1978)
—
$30.87*
$46.30*
20%
$9.26*
They calculated $6.17 per capita
in savings to residence owners.
Assumed residential costs were
two-thirds of total costs.
Bennett et al.
(1979)
(cited in Ryder,
1980)
$9.40
—
$28.20*
20%
$5.64*
Assumed that 200 million people
are served by public water system
and that distribution costs were
one-third of total costs.
Energy & Environ-
mental Analysis
(1979)
$3.98
$7.97
$11.95
38%
$4.54
This is an admitted underestimate
it includes only damage to pipes
(not damage to water heaters,
increased operating' costs, etc.)
Ryder (1980)
$1.17
$22.19
$23.36
25%
$5.84
Ryder ascribed 95% of corrosion
damage to private owners.
Kirmeyer & Logsdon
(1983)
$23.60*
$35.40*
40%
$14.16*
Assumed residential costs were
two-thirds of total damage.
AVERAGE $8.21
W/OOT EEA $8.82
* These estimates have been calculated by the authors of this paper. Assumptions are noted above.
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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.B.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/l could
produce annual net benefits of about $800 million in 1988.
It should be enqphasized 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
$27.6 million
$81.2 million
$268.1 million
$108.8 million
$295.7 million
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
$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/l to 20 ug/l for Sample Year 1988
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 carpensatory education
- children at risk of stature decrement
- fetuses at risk
- increased risk of hematological effects
Reductions in Numbers
of People at Risk
42 million*
29,000
230,000
11,000
100
29,000
82,000
680,000
82,400
Mult health benefits
-cases of "hypertension
(males, aged 40-59)
-heart attacks
{white males, aged 40-59)
-strcSces
(vfciite males, aged 40-59)
-deaths
(white males, aged 40-59)
-(reduced risk to pregnant wcmen
((woman, 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.e. 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.
Boston1s water is highly corrosive: it is relatively acidic
(pH = 6.7) and soft (14 mg/1 as CaCC>3), 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., 1975i 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 benefits
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:
° 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?
° 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
° 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 mater ials
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/l (Lovering, 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.1. 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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11-4
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 cond itions typical in pr ivate 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 pr ivate homes is
heated, greatly increasing its corrosive potential.
II.A.l.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? She iham 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? Love11 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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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 (01iphant, 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 CaCOj)
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. 01iphant (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 stand ing 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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II.A.I.e. Lead Pipes
Several characteristics of lead piping also influence lead
levels in drinking water (Pocock, 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; Pocock,
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
XI.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 corros ive 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; Pocock, 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; Kuch 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
t imes 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., 198 5; 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/l and are usually below 20 ug/l.*
II.A.2. Prevalence of Lead Materials in Distribution Systems
Lead lias 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/l (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/l, with a
mean level of 43 ug/l (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 §141.1(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.l. 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 EPA's 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 , sod ium , pH, alkalinity, chloride , conductiv ity ,
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, 1ithium 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 1iquid 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 ind icated 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. Fi fty-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 li-l.
II.B.l.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/1)
< 10 11-19 20-49 > 50
Percent of samples 60 24 13 3
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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 CaC03 (roean, 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. Geolog ical 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.+ It is log ical
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 J50 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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The Culligan data portray higher levels of lead contamination,
however, than do either- EPA'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 EPA's 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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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 dr inking water.
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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 'dirtier' 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 in formed 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 1ikely and
did, in fact, occur. Not surprisingly, because the samples were
taken by a water softening company, overall hardness results from
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11-27
the Culligan/Patter son 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 (19835 have shown,
however, that at a pH of 8-8.5, soft water (i.e., 30 mg/1 as CaCO^)
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 signi ficant
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 Reg ion, 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 % Population* % Samples
Northeast States
CT 1.4 0.63
MA 2.5 2.4
ME 0.4 0
NH 0.4 0.38
N J 3.3 5.2
NY 7.8 5.3
PA 5.3. 3.9
RI 0.4 0.50
VT 0.2 0.25
Total 22% 19%
Southeast States
DE 0.3 0.25
PL 4.3 2.9
GA 2.4 1.8
MD 1.9 1.3
NC 2.6 0.25
SC 1.4 0.63
VA 2.4 2.6
WV 0.9 2.4
Total 16% 13%
Midwest States
IA 1.3 3.7
IN 2.4 6.2
IL 5.1 12 • 4
KS 1.0 1.9
MI 4.1 2.0
MN 1.8 4.2
MO 2.2 2.3
ND 0.3 0.38
NE 0.7 1.3
OH 4.8 4.6
SD 0.3 0.76
WI 2.1 2.0
Total 26% 42%
* U.S. Bureau of Census, 1980. In the Patterson study, 1978 Census
data were used.
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11-31
TABLE II-2, (Continued)
State % Population* % Samples
Southcentral States
AL
AR
KY
LA
MS
OK
TN
TX
Total 17% 11%
Western States
AZ 1.2 2.0
CA 10.5 2.3
CO 1.3 6.3
ID 0.4 0.51
MT 0.3 0.88
NM 0.6 0.88
NV 0.4 0.51
OR 1.2 1.3
UT 0.6 0.25
WA 1.8 0.13
WY 0.2 1.0
Total 19% 16%
1.7
1.0
1.6
1.9
1.1
1.3
2.0
6.3
0.25
0
1.0
1.3
0.63
0.88
1.8
5.2
* 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.l.
** 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/l as CaCC^); 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/l as CaCOj). 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, 19 75; 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/l vs. 12 and 24 mg/l,
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/l 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/l (from lead
solder alone? there were no lead pipes) and in the latter, mean
lead levels were over 100 ug/l 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/l as CaC03) often result in lead contamination
levels exceeding 50 ug/l* 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/l, 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/l as CaC03), half of first-
flush samples could exceed 20 ug/l, and that 10 percent of them
could exceed 50 ug/l.
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/l in first-
flush samples and many also had levels > 20 ug/l 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/l =
17% of population exposed to water >20 ug/l
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/l. The results are most sensitive to the estimate of
lead levels > 20 ug/l. (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/l.)
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/l, with a home occupied for only three months having lead
levels of _> 100 ug/l. 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 Port Collins (Colorado).
The results from Little Thompson showed one-third of the residences
sampled exceeded 20 ug/l — 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/l) was in a not-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/l, 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/l in 15 states plus the District
of Columbia. This shows that the occurrence of lead levels
exceeding 20 ug/l 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/l as CaC03), 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/l as CaCOj) 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)
Mean Pb
% of
Age of
Level
Samples
Study
Housing
(ug/1)
>2.0 ug/1
Conditions/Notes
Sharrett
<18 months
74
NG
(Median standing levels
et al.
<5 years
31
NG
(No lead pipes
(1982a)
>5 years
4.4
NG
(
Nassau
unoccupied
2,690
NG
(Average, first flush
County (1985)
<2 years
540
NG
(
2-10 years
60
NG
(
>10 years
10
NG
(
Philadelphia
<2 years
90
NG
Flushed
(1985)
5000
NG
First-flush
>2 years
60
NG
Flushed
500
KG
First-flush
>4.5 years
<25
NG
NG
EPA (1987)
<2 years
NG
93%
First draw (pH <6.4)
preliminary
N3
51%
Flushed, 2 minutes (pH <6.4)
results
<2 years
NG
83%
First draw (pH 7.0-7.4)
NG
5%
Flushed, 2 minutes (pH 7.0-7.4)
<2 years
NG
72%
First draw (pH >8.0)
NG
0%
Flushed, 2 minutes (pH >8.0)
2-5 years
NG
84%
First draw (pH <6.4)
NG
19%
Flushed, 2 minutes (pH <6.4)
2-5 years
NG
28%
First draw (pH 7.0-7.4)
NG
7%
Flushed, 2 minutes (pH 7.0-7.4)
2-5 years
NG
18%
First draw (pH >8.0)
NG
4%
Flushed, 2 minutes (pH >8.0)
>5 years
NS
51%
First draw (pH <6.4)
NG
4%
Flushed, 2 minutes (pH <6.4)
>5 years
NG
14%
First draw (pH 7.0-7.4)
NG
0%
Flushed, 2 minutes (pH 7.0-7.4)
>5 years
NG
13%
First draw (pH >8.0)
m
3%
Flushed, 2 minutes (pH >8.0)
KEY: Pb = Lead
N3 = Not given
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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/l. 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/l 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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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/l of lead or greater.
II.C.l. 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/l, 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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Assumption: Treatment can generally reduce lead levels to 20 ug/l.
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 (DIC) as opposed to alkalinity,
because DIC is independent of pH while alkalinity is not. These
studies found that increasing DIC 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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®BLE II-4. Percentage of Samples Exceeding 20 ug/1 of Lead at Different
pH Levels, by Age of House
Percent of samples >20 ug/1
Age of House pH First-flush Fully-flushed (2 min)
0-2 years £6.4 93% 51%
7.0 - 7.4 83% 5%
>8.0 72% 0%
2-5 years <6.4 84% 19%
7.0 - 7.4 28% 7%
>8.0 18% 4%
6+ years £6.4 51% 4%
7.0 - 7.4 14% 0%
<8.0 13% 3%
Sources U.S. EPA (1987), preliminary results frcm "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, ind icate 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 monitor ing 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 cr iteria for compliance with the new MCL
will consider the risk of contamination by corrosion by-products.
A revision of EPA's monitor ing requirements was called for by the
cour t 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 beg inning 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 1inear forms cited above
and used in this analysis provide results similar to the non-1inear
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., 19 83; Bailey and Russell, 1981). This seems counter-
intuitive at first because the intake of stand ing 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
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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 var ies 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.
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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. Cur iously, 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 contr ibutions 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).
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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 198 3; 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
1imit 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.
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11-52
that new solder would on average produce lead levels at half the
MCL, i.e., 25 ug/l, 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 1 per day — one in the morning and the other when the
* Or its equivalent; Some first-flush and some fully flushed
water.
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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.
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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
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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 (19855 U.S. residential population
* Survey of Current Business, U.S. Department of Commerce -
Bureau of Economic Analysis, 1985; Table on New Housing
Construction.
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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.
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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 mill ion, 219.2 mill ion are served by community water
systems. Again, we assumed that the people who live in new
housing (9.6 mill ion) are distr ibuted 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 mill ion) 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.
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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
° because it does not include the potential exposure
of occupants in housing built within the past 2-5
years;*
° 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;
° 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.
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11-59
° 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
° 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.
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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-1, 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
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III-2
Fiqurs III-l Multi-Organ Impacts of lead's
Effects on the Heme Pool
REOUCTIONOF
KIMCBODVPOOl
fftVTHftOPQIEtlC
effects en neurons,
AXONS, AND
SCHWANN CIUS
Mid AL-cnoocnmc
HEPATIC
EFFECTS
HVOROXVlATION
Of CORTISOL
IMPAIRED
OE TOX1F1CATIQN
or xenoijotics
ANEMIA-REQUCED
OXVCEN TRANSPORT
TO AU TISSUES
OlSTURBED IWUNO
REGULATOR* R0«
Of CALCIUM
OISTURIEO ROLE IN
TUM08ISENESIS
CONTROL
OISTURBEO CALCIUM
METABOLISM
REOUCIO UHOM)2 -
VITAMIN Q
IMPAIRED DEVELOPMENT
Of NERVOUS SYSTEM
REDUCED KEMOmQTElNS
CYTOCHROMES!
IMPAIREOMITAIOIISM
IMPAIRED MYEMNATION
ANONERVE CONDUCTION
REOUCEO HEME FOR
HEME REGULATED
TRANSFORMATIONS
IMPAIRED CALCIUM
ROLE AS SECOND
MESSENGER
IMPAIRED CALCIUM
ROLE IN CYCLIC
NUCLEOTIDE METABOLISM
EXACERBATION OF
HVFOXIC EFFECTS OF
OTHER Sf RESS AGENTS
IMPAIRED MINERAL
TISSUE HOMEOSTASIS
IMPAIRED
DETOXIFICATION
OF ORUCS
IMPAIRED OETOXIFICATIOH
OF ENVIRONMENTAL
CAROIOVASCUIAR
OVSF UNCTION ANO
OTHER HVFOXIC EFFECTS
AITlRlOMETABCf ISM
Of TRYPTOPHAN
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LEVELS OF TRYPTOPHAN.
SEROTONIN. ANOMIAA
MPAIRf 0 BONE ANO
TOOTH DEVELOPMENT
OlCfURlEO INOOLEAMlNE
NEUROTRANSMITTER
FUNCTION
Multi-organ impact of reductions of heme body pool by lead. Impairment of heme
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 (—
-------
FIGURE III-2. SUMMARY OF LOWEST OBSERVED EFFECT LEVELS FOR KEY LEAD-INDUCED HEALTH EFFECTS IN CHILDREN
Lowest Observed Heme Synthesis and 13 Neurological Renal System Gastrointestinal
Effect Level (PbB) Hematological Effects Effects Effects Effects
80-100 ug/dl
Encephalopathic Chronic nephropathy
signs and symptoms (aminoaciduria, etc.)
Colic, other overt
gastrointestinal
symptoms
1
70 ug/dl
Frank anemia
I
1
V
60 ug/dl
Peripheral neuropathies
50 ug/dl
?
40 ug/dl
Reduced hemoglobin
synthesis
Elevated coproporphyrin
Increased urinary ALA
CNS cognitive effects
(IQ deficits, etc.)
Peripheral nerve
dysfunction
(slowed NCV's)
30 ug/dl
Vitamin D metabolism
interference
l
15 ug/dl
Erythrocyte
protoporphyrin
elevation
l
Altered CNS I
electrophys iolog ical 1
responses I
i |
10 ug/dl
ALA-D inhibition
j I
V V
? ?
Py-5-N activity
inhibition
1
V
?
Abbreviations: PbB = blood lead concentrations; Py-5-N = pyrimidine-5'-nucleotidase; CNS = central nervous system;
NCV = nerve conduction velocit; ALA = aminolevulinic acid
Source: Air Quality Criteria Document for Lead (1986)
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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 cost-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.
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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-
tionalized 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).
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III-6
III.A. Pathophysiological Effects
—PH-— IfiM I H .1 a I
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
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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
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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)
10-19 20-29 30-39 40-69
<10 uq/dl uq/dl uq/dl uq/dl uq/dl
All Races
all ages 22.1 62.9 13.0 1.6 0.3
6 months-5 years 12.2 63.3 20.5 3.5 0.4
6-17 years 27.6 64.8 7.1 0.5 0.0
White
all ages 23.3 62.8 12.2 1.5 0.3
6 months-5 years 14.5 67.5 16.1 1.8 0.2
6-17 years 30.4 63.4 5.8 0.4 0.0
Black
all ages 4.0 59.6 31.0 4.1 1.3
6 months-5 years 2.7 48.8 35.1 11.1 2.4
6-17 years 8.0 69.9 21.1 1.0 0.0
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Ill—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 (EEG) 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 EEG
patterns appear to persist over a two-year period.
Also, the relative amplitude of synchronized EEG
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.
-------
III-10
7. An inverse relation between maternal and fetal
blood-lead levels and gestational age, 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.l. 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 iri 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 (Litraan 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-(OH52 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.y Rosen et al.,
1980ar 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., 1980bj 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.
-------
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
-------
111-16
immunoregulatory cells, such as monocytes and activated lymphocytes
(Provvedini et al., 1983; Bhalla et al., 1983).
The negative correlation between blood lead and serum
1,25-(OH52 vitamin D, 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 rn vivo and iji 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
-------
111-17
and modulate the metabolism of steroid hormones (Goldberg et al.,
1978; Saenger et al., 1984),
While cytochrome P-4 50 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 assoaiation
-------
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 ^nd 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.
-------
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 sme11ing 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
-------
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]."
-------
Ill—21
Since then, however, surprisingly few studies have investigated
this effect, until quite recently.
In the 1970s, three studies (Mooty et al., 1975 7 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.
-------
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.
-------
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).
-------
111-24
FIGURE III—3 Relationship of Blood Lead Level to
Weight in Children Aged 0 to 7
170
16 •
161
16 4
160
1&I
156
ADJUSTED HOOD LEAD (utftll)
Adjusted weight and adjusted blood lead levels for children aged 7 years and
younger in Second National Health and Nutrition Examination Survey. Both weight and
blood lead level have been adjusted by regression for effects of age, race, sex, and all other
variables significant at .05 level. Each point is mean weight and mean blood lead level of
approximately 70 consecutive observations, ordered by blood lead levels. Regression line
reflects slope of coefficient obtained from multiple regression analysis of all 1,987 obser-
vations with no missing data.
Source; Schwartz et al., 1386.
-------
111-25
FIGURE III-4 Relationship of Blood T^n Level to
Height in Children Aged 0 to 7
ADJUSTED
MEiGMT lew!
106.25
• «
107.00
106 00
106 00
20
ADJUSTED BLOOD LEAD (uf/dl!
Adjusted height and adjusted blood lead levels for children aged 1 years and
younger in Second National Health and Nutrition Examination Survey, Both height and
blood lead level have been adjusted by regression for effects of age, race, sex, and all other
variables significant at .05 level. Each point is mean height and mean blood lead level of
approximately 100 consecutive observations, ordered by blood lead levels. Regression line
reflects slope of coefficient obtained from multiple regression analysis of all 2,695 obser-
vations.
Source; Schwartz efc al,r 1986.
-------
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 neurotoxleant 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.l. 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.
-------
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 EEG 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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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.
III.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) .
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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?
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111-33
Yule, 1984), as well as persistent abnormal EEG 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 (Otto 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
in 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 j itteriness 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
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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,
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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
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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.l. Assessing the Benefits of Reduced Fetal Exposure to Lead
Lead crosses the placental barrier and fetal uptake of lead
continues throughout development. Fetal 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 iri 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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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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II1-47
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.
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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 assumption: 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.
III.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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III.D.1. 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 Pediatries (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-tetraacetic 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 chelation 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
no
yes
no
no
NOTES:
^Provocative EDTA. or
other test
yes
tChelation therapy, because
of its severe side-effects
and inherent dangers, cannot
be repeated again after this
sirtple
follow-up
long
follow-up
elevated
EEP?
chelation
therapy
repeat
chelation?
high body
lead burden?*
Blood Lead Levels
>25 ug/dl
point
long
follow-upt
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111-52
TABLE III-2. Percent of Children Requiring Chelation Therapy
Blood Lead Levels Pereent
25-30 ug/dl 0*
30-39 ug/dl
age three and over 9.6*
age under three 11.5*
40-49 ug/dl
age three and over 26.0
age under three 37.9
50-59 ug/dl
age three and over 36.0
age under three 49.0
above 59 ug/dl 100.0
Source: Piomelli et al., 1984
* At blood lead concentrations of 25 to 35 ug/dl, 6-7 percent of
children require chelation 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 chelatable lead, it is possible that some
children between 15 and 24 ug/dl (a concentration below CDC's
definition of 'elevated' 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 Pediatries, 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 under 30 ug/dl to a high of 100 percent
for those over 59 ug/dl.
Based on the data from the NHAN1S II, 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 pereent of
the children above 25 ug/dl would require chelation therapy.
In addition, we estimated that half of those children chelated
would require a second chelation due to a rebound in their blood
lead level, and that half of those children would require a
third chelation treatment. Thus, a total of 0.0875 chelations
would be required for every child over 25 ug/dl blood lead at
screening. To calculate the total cost per chelation, we estimated
that it would require five days in the hospital, several physieians'
visits, laboratory work, and a neuropsychological evaluation,
for a total cost of about $2,700 per chelation.
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 (sueh as work
time lost by parents), the adverse health effects of chelation
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 fo'llow-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.
-------
111-58
reducing a child below 30 ug/dl could increase earnings by 1.0
percent
(0.9% x 4 IQ points t 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 t 3.5 years = 1.3%).
The present value of expeeted 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 expeeted 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
expeeted 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 foree 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.
-------
II1-59
TABLE III-3. Estimated Annual Benefits of Reduced IQ Damage
by Using Changes in Expected Future Lifetime
Earnings, For Sample Year 1988
Blood Lead Level
15 ug/dl
30 ug/dl
50 ug/dl
TOTAL
Number of children 230,000
IQ points
potentially lost
1-2
per ehild
Present value of $1,040
decreased earnings per ehild
(1985 dollars)
11,000
$2,600
per ehild
100
per ehild per child
$3,350
per ehild
241,100
NA
NA
TOTAL
(1985 dollars)
$239.2
million
$28.6
million
$ 0.3
million
$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 eonsequenee
of lead1s 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 ehild were not calculated.
Instead, we calculated the annualized benefit from avoided 10
losses of reducing 230 ,000 children below 15 ug/dl; 11 ,000 chiIdren
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 ehild
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, effect's
upon future ability and performance eould 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)
METHOD 1
Medical Compensatory Total
Expenses Education Costs Method 1
Number of
children 29,000
Costing
unit
Total
benefits
$950
per child
$27.6
million
29,000
$2,800
per ehild
$81.2
million
29,000
$3,750
per ehild
$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.
Ill.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. In 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
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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 incapacitation (including behavioral dis-
orders) from lead's adverse effects upon virtually every human
systemj 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 neurotoxicity. 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 pathophysiological and neurotoxic
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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I11-68
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)
° Medical costs
° Cognitive damage costs:
ccrrtpensatory 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;)
° Requiring medical treatment
° Loss of 1-2 IQ points
4 IQ points
5 IQ points
° Requiring compensatory education
° Stature decrement
° Fetuses at risk
° Increased risk of hematological effects
29,000
230,000
11,000
100
29,000
82,000
680,000
82,000
-------
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
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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.h.1. 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).
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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.l.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.
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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
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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.I.e. 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).
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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
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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.
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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.
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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
def initively.
"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)
Available in the Central Docket Section of EPA. Docket number,
ECAO-CD-81-2; documents numbered IIA.F.60, IIA.C.5, II.A.C.9,
and IIA.C.11 .
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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
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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 be ing associated most clearly
with blood pressure increases, but certain evidence
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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
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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.
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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)
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IV-17
.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...
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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 (All),
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
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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 1iver function. In
the remaining three dogs, renin secretion increased? this
was thought to be due to lead activation of normal mechanisms
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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...
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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
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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
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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.
"In vivo tests of cardiovascular reactivity in rats
exposed to 50 ppm lead (blood lead 38.4 + ug/dl) for 160
days were performed by Iannaccone 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 rn vitro system for
monitoring the cardiac electrical conduction system
(electrocardiogram or ECG) and systolic tens ion, and
demonstrated that jin 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 ECG... [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...
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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-2 5
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)
.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 Kobayashi1s 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
'soft'. Most studies investigating CVD and water hardness have
focused upon systems with very soft water, i.e., _< 40 mg/1 as
CaC03.
-------
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 weire
"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 arteries*.
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.
-------
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.
Interest in identifying a 'water factor' 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 eorrosive water.
Or soft water may initiate heart disease, or soft water parameters
added onto other faetors 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,
whieh costs $65,000 per case.
-------
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.
1) 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.)
-------
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.3.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.
-------
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.
-------
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
-------
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 case, 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.
-------
IV-3 5
in blood pressure over the past decade arid 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, 1986j
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 whites.
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
-------
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 epidemio-
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 myocar-
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 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-3 9
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 Pramingham 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
myocardial 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 abortifacients 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
-------
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.
-------
IV-4 3
IV.B.l. 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)
-------
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 case.
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 throughout
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.
-------
IV-4 5
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 mill ion 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-4 6
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-4 7
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-4 9
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. S ince 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 Ml 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 $15,230 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
TABLE IV—1. Benefits of Reducing Strokes (1985 dollars per case)
Total
Type of Stroke
Age
i
Medical
Expenses
Foregone
Earnings
Hemorrhagic
35-44 $13,600
44-54 14,300
55-64 18,600
Infarctive
35-44 19,000
45-54 19,600
55-64 25,500
Transient ischemic attacks
35-44 3,450
45-54 3,450
55-64 3,450
$44,300
28,100
11,900
76,700
46,500
15,100
1,200
3,325
8,950
$57,900
42,400
30,500
95,700
66,100
40,600
4,650
6,775
12,400
Weighted average
$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
1976i 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. Summary of Annual Monetized Blood-Pressure
Related Benefits of Lowered MCL For Sample Year 1988
Category
Unit
Cost Annual
Sub-Population (1985 Avoided
Considered dol lars) Cases
Total Benefits
(millions
1985 dollars)
Cases of hypertension
Myocardial infarctions
Strokes
Deaths
males,
aged 40-59
white males,
aged 40-59
white males,
aged 40-59
white males,
aged 40-59
$250
$65,000
$48,000
$1 million
130,000
240
80
240
$32.5
$15.6
$3.8
$240.0
TOTAL
(millions 1985 dollars)
$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 ares
- kidney effects, detectable in children at blood lead
concentrations of about 10 ug/dl, although the damage is
often not manifest unti1 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
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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 af 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-monetized
Health Benefits of Lowered MCL For Sample Year 1988
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
$250
$65,000
$48,000
white males, $1 million
aged 40-59
130,000
240
80
240
$32.5
$15.6
$3.8
$240.0
$291.9
NON-MONETIZED FEMALE REPRODUCTIVE EFFECTS
Adverse reproductive
effects
(Pregnancies at risk)
(of adverse effects )
( - same as at-risk )
( fetuses )
women, NA 33,000
aged 15-44
>15 ug/dl
pregnant women, NA 680,000
aged 15-44
NA
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 water'), 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
corrosiv ity. 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,
m* ^ 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 CaC03)-or very high alkalinity (> 150
rag/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 (CaC03) 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
CaCC>3 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 wi11 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 Lanqelier Saturation Index (LSI) or Lanqelier 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 CaC03
would be at saturation concentration. The saturation value of the
water with respect to CaC03 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 CaC03; a value of zero indicates equilibrium.
In other words, a positive LSI indicates a tendency for the water
to deposit a protect ive CaCC>3 layer on the pipe, and hence impede
corrosion. Negative values indicate a water's tendency to dissolve
CaCC>3 from the pipe1 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 draw* water can be several times higher than in 'running'
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 aggress ive 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
-------
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 CaCC>3): 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—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 CaC03) and that the median
U.S. drinking water is about 91 mg/l-CaC03. Another paper
(Greathouse and Craun, 19-78) 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 > 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
-------
V—19
distributed in the U.S. is naturally corrosive, and is either
untreated or, for whatever reasonfs), 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/l as CaCC>3, 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.
** Thif? issue is discussed in Section II.B.l., 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 manv times hinher.
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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
t
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 MR I (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 1 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 Seattle1s 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 Seattle1s 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.
-------
V-30
T&HLF, V-l. Estimates of Annual Per Capita Corrosion Damage (1985 dollars)
Corrosion
Studies
Estimated Annual Corrosion Damage
(per capita)
Damage
Avoidable
Through
Welter
Treatment
Annual Per
Capita Benefits
of Corrosion
Control
Assumptions/Notes
Distribution
Systems
Residential
Total
Kennedy Engineers
(1973)
$5.57
—
$16.71*
30%*
$5.01*
Assumed 30% potential reduction
in corrosion damage and that dis-
tribution costs were one-third of
total costs.
Hudson & Gilcreas
(1976)
$8.68*
$26.04*
50%
$13.02*
They did not include increased
operating costs. Per capita
estimate assumes 200 million
peqple are served by public water
systems. Assumed that distri-
bution costs were one-third of
total costs.
Kenned/ Engineers
(1978)
—
$30.87*
$46.30*
20%
$9.26*
They calculated $6.17 per capita
in savings to residence cwners.
Assumed residential costs were
two-thirds of total costs.
Bennett et al.
(1979)
(cited in Ryder,
1980)
$9.40
—
$28.20*
20%
$5.64*
Assumed that 200 million people
are served by public water systems
and that distribution costs were
one-third of total costs.
Energy & Environ-
mental Analysis
(1979)
$3.98
$7.97
$11.95
38%
$4.54
This is an admitted underestimate:
it includes only damage to pipes
(not damage to water heaters,
increased operating costs, etc.)
Ryder (1980)
$1.17
$22.19
$23.36
25%
$5.84
Ryder ascribed 95% of corrosion
damage to private owners.
Kinneyer & Logsdon
(1983)
$23.60*
$35.40*
40%
$14.16*
Assumed residential costs were
two-thirds of total damage.
AVERAGE $8.21
W/OJT EEA $8.82
* These estimates have been calculated by the authors of this paper. Assunptions are noted above.
-------
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.
-------
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, 19865. 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 (US-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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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) Teacher1s
ratings of children's behaviour in relation to blood lead levels.
British Journal of Developmental Psychology.
-------
APPENDIX A: 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/Ls
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
-------
TABLE OF CONTENTS
EXECUTIVE SUMMARY . Pag© i
INTRODUCTION - Page 3
BACKGROUND Page 5
BOSTON: ITS WATER AND CURRENT TREATMENT Pag© 12
PROPOSED TREATMENT AND ITS COST Page 15
HEALTH BENEFITS Page 20
CHILDREN'S BENEFITS Page 22
HEALTH BENEFITS — ADULT WHITE MALES, AGES 40-59 ... Page 26
Hypertension . Page 28
Cardiovascular Disease Page 28
Myocardial Infarctions. . . . Page 23
Strokes 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
-------
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 (e.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 1388).
The results of the analysis suggest that EPA should take the
fol1owing actions:
1, Lower the maximum contaminant 1 ever
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 1evels of lead and
other contaminants in drinking water.
-------
INTRODUCTION
Since 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/.-ault 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 30 pg/dl to 25 pg/dl (when coupled
with free erythrocyte protoporphyrin . 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
-------
4
plumbing by corrosive water.1 Treatment methods now being used
in some communities have reduced lead concentrations below the
current MCL of .05 nig/L. If a new, lower standard is adopted,
though, addi t ional 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
bo the benefits. Because of data and epidemiological
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
1 U.S. Environmental Protection Agency, "Regulating Corrosive
Water", Office of Planning and Evaluation, April 1981, p.2.
-------
comparison and discussion of the costs and benefits and
r ec omrnendat 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.3
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 , Internal Corrossion of
Water Distribution Systems; Cooperative Research Report. 1985. p.
214.
3 U.S. EPA, "Statement of Basis and Purpose for Amendments to the
National Interim Primary Drinking Water Regulations", Office of
Drinking Water, 1980, p. 48.
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6
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,
caul king, gaskets, solder and plumbing fixtures."*
Although solder and plumbing fixtures constitute
proportional1y 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 1377 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.®
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 '35'®^
Annual Conference, Minneapolis, Minnesota,June 9-12, 1975, p. 7.
5 AWWA, Op. cit¦. p.215
S 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, 1SS5.
8 AWWA, Op. cit.. p.222
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7
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
water, In two studies, one by Millette and the other by the
Midwest Research Institute
-------
3
carbonate CCaC035. In hard waters, where high concentrations of
CaC03 are present, a protective skin forms along the inner walls
of pipes. •*SE Soft water tends to be corrosive because the CaCQs
concentration is low which inhibits the formation of the
protective film. M:a
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. 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.
12 Ibid., pp.31-32
13 Ibid., p.35
t4 U.S. EPA. "Regulating Corrosive Water", 1981,p.S.
15 Ibid., p.S.
16 U.S. EF'A, Costs and Benefits of Reducing Lead in Gasoline.
1385, chapter IV.
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3
Studies from the mid—1970's have suggested vhat there is a
relationship between soft water and cardiovascular disease t:C"VD!> .
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, 1eachate contaminants
common is soft water such as lead can increase blood pressure,
•and with it, the incidence of CVD. 1,r 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 37% 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 controlling
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"*
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 to
the National Interim Primary Drinking Water Regulat ions", p.45.
18 Pirkle et. al., "The Relationship Between Blood Lead Levels
and Blood Pressure and its Cardiovascular Risk Implications",
American Journal of Epidemeology, 1985, 121:246
19 U.S. EPA, "Statement of Basis and Purpose for Amendments to
the National Interim Primary Drinking Water Regulations", p.26.
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10
protective CaCOs* 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 cites 1aboratory 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.22
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.
-1 AWWA, op. c i t.. p.243
22 Ibid.. pp.246-260.
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i 1
hypertension in animal studies.asa Cadmium also may cause
irreversible renal damage.®"* 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.®® 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.
Finally, corrosive water damages pi pes 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.Q.
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.
26 Bureau of Water Works, Por11 and,Oregon, Internal Corrosion
Mitigation Study: Final Report. 1982, p.5-12.
27 U.S. EPA, "Regulating Corrosive Water", p.13.
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33% of the water supply.3"* In addition, corrosion promotes
tuberculation, a process in which leached materials build up on
the inner walls of pipes reducing their carrying capacity.*"5*
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 £.7, and soft with hardness
measured at 12 mg CaC03/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 recognized 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 t z<
the National Interim Primary Drinking Water Regulations", p.27.
29 U.S. EPA, Regulating Corrosive Water, p.13.
30 Karalekas et. al., "Control of Lead, Copper, and Iron Pipe
Corrosion", Journal of the American Water Works Association,
1383, p.93.
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CBWSC) estimate that 44% of their residential customers still
have lead services.34
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. a=* 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 th* mid 1970's.
This study revealed a large proportion of samples in excess of
the- .05 mg/L MCL.3a» 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, 198S.
32 Karalekas, "Lead and Other Trace Metals in Drinking Water in
the Boston Metropolitan Area", p. 7.
33 Ibi d. , p. 13.
34 Worth et. al. "The Contribution of Household Tap Water to
Blood Lead Levels", U.S. EPA grant # R-802794, 1981, p.20.
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14
At first, the MDC used zinc or triphosphate 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 (NaOH), 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 signi ficantly lower for NaOH tr eat merit. 37' In addition,
sodium levels in MDC water were sufficiently low that adding
sodium would not create a health problem.3"
Monitoring performed by EPA's Region I office from 1976 to
1981 indicated that lead, iron and copper levels dropped
signi f icantly. 3<* More important 1 y, lead levels in most water
samples fell below .05 mg/L. Most samples, however, had levels
which remain above the contemplated .01 mg/L MCL. Cr-.-np 1 iance
with the proposed standard will require corrosion control to
further reduce lead levels in Boston's drinking water.
35 Karalekas, "Control of Lead, Copper, and Iron Pipe Corrosion",
p. 94.
3£ Discussion with Peter Karalekas and studies reported in the
AWWA corrosion control study, December, 1985.
37 Discussion with Peter Karalekas, April,1936.
38 Ibid.
39 Karalekas, "Control of Lead, Copper, and Iron Pipe Corrosion",
p. 93.
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IS
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 rng/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 services, 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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16
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. *'y First, MWRA would further raise pH' by increasing
the NaOH concentration. When the MDC first began NaOH treatment,
the state of the art suggested that pH should be elevated to a
range of 7 to S 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 throughout 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 sine orthophosphate was a likely scenario,
December, 1985.
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17
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 mg/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 to those used for ch1 or i nat i on
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 <:0S
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18
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 bo the desired level.
Both the EPA and MWRA estimate that chemical costs would increase
by approximately 10%. Because NaOH is a by-product of automobile
rnanufactur ing and output vari es directly with automobile output,
its price has fluctuated dramatically. Based on the average
price for the last five years, the cost of NaOH is *.34 per mg
per million gallons Cmg/MQ, 1985*).At that price, raising
chemical costs by 10% would amount to an annual incremental
increase of $85,000 (1985 *f all costs and benefits in this paper
are in 1985 * unless otherwise specified), assuming an average
flow of 310 million gallons per day CMGD).
The cost of an additional two 50 MQD NaOH feed systems
including installation is * 150, 000. ***• Amortised at 5% over 20
years, the resulting annual capital cost is *12,000. Operating
and maintenance costs are *30,000 (207. of *150,000). Therefore
phase I would cost approximately *127,000 per year, (See TABLE I
for a summary of treatment costs.)
Although the per unit chemical cost for zinc orthophosphate
is much higher, its feed rate tends to be low. While the
literature cites several different cost estimates, bhis study
43 NaOH cost figures supplied by the MWRA.
44 U.S. EPA, "Corrosion Manual for Internal Corrosion of Water
Distribution Systems", Prepared for the Office of Drinking Water
by Environmental Science and Engineering, Inc., 1984, p.103.
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TABLE I
TREATMENT COSTS
PARAMETERS
average flow 310
interest rate 5%
payback period 20
CRF 0.08024
NaQH
cost
$5. 44
EPA (B)
cost (mg/MQ)
feed rate Crng/L)
$5.44
Tech Products
coat /MQ > s21 - 00
f *ed rats Cmg(Zn>/L> 0.6
cherni cal s
0*M
capital
total
$ 1, 231, 07'2
*34,000
$13,641
$1,278,713
; h efi'i i c a 1 s
O&M
capital
total
£1, 846, SOS
$34,000
313,641
$ I • 394, 24'S
O&H
cap ital
b o t •?. a
*i,425,690
o 0 f C.'U
S12,036
$ .1 , 467, 726
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TABLE I Ccorrb.)
AWUIA
cost C mg CZn>/MS) $19.20
feed rate
-------
19
uses the- figures provided by Technical Products, a chemical firm
which manufactures orthophosphate and supplies the feed systems.
Assuming a flow of 310 MGD and a feed rate of .6 mg/L, the annual
chemical cost is $1,425,000 based on a uni t cost of $21 per rug of
sine per million gallons (mg
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HEALTH BENEFITS
Despite the fact that the health effects from exposure to
lead are relatively well understood, monetizing 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 Region 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, fche decline in lead
concentrations ranges from .05 mg/L to .0055 mg/L for the
households in the sample.
-------
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 Conly 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, in
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 organised 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.**® 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 nest decade as the
baby-boomers age.
Finally, when estimating health benefits, this analysis
assumes that the proposed MCL will not be implemented until at
least 1988. Thus, the calculations reflect benefits starting in
that year and extending out to 1992.
CHILDREN'S 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 EF'A's
45 Boston Redevelopment Authority, "Popul at i on" 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, 19S5, pp.41-44.
-------
study of 1ead in gasoline. The derivation of avoided costs is
based on the number of children whose blood lead level falls
below 25 j.tg/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
*
starting with six months to the second bi rthday and ending with
twelve to thirteen years of age.** MINITAS, 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 1983 study by Ryu which established
the r el at i onshi p between water lead and blood lead in children as
depicted in the following equations
PbB = a + . 12F'bW
where:
PbB = blood lead in pg/dl;
a = the constant plus other demographic and
other environmental factors; and
PbW - water lead in pg/L (standing grab
samp 1 e•
46 Children Were categorised in this way because blood lead
distributions are heavily dependent on age and race.
-------
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 .66 pg/dl to 6.04 pg/dl depending on
the reduction in water lead in his/her household.
In the final step, a BASIC program used the initial b1ood
lead di str i but ions and epidemiological relationship above to
simulate the change in the blood lead distribution for each
age/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 1988 Csee Table II).
In berms of medical and compensatory education expenses, EPA
believes that $3,900 can be saved for each avioded case of lead
poisonings $1,100 for medical treatment and $2,800 for education.
Therefore we can expect a total of $340,000 in benefits for
children in 1988, 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 «: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 proportional1y fewer
individuals with blood lead >25 pg/dl thus reducing the
-------
TABLE II
CHILOESS'S BENEFITS
AHETERS
*fit per capita 13,900
ippi 1 c io 1 e 541
BLACKS
•::£
! CHANGE
NUMBER
BENEFITS
BENEFITS
BENEFITS
BENEFITS
BENEFITS
Sati?
POP
25 M/dl
CHILDREN
1988
POP
1989
POP
1990
POP
1991
POP
1932
;-<2yr
4274
0.530%
12.2
147,706
4329
$48,319
4385
$48,944
4390
$49,000
4396
$49,067
2-3
571?
0.7152
22.1
186,086
5772
186,914
5850
$88,089
5855
$88,164
5861
$88,254
*-3
5350
0.7052
20.4
*79,433
5384
$79,938
5416
$80,413
5467
$81,170
5495
$81,586
4384
0.3102
8.3
132,539
4995
$32,610
5001
$32,650
5078
$33,152
5143
$33,577
5-9
4618
0.0852
2.1
18,267
4607
$8,247
4S79
$8,197
4690
$8,396
4784
18,564
iO-11
4251
0.0002
0.0
to
4218
$0
4163
$0
4292
$0
4422
$0
12-13
3885
0.0052
0.1
$409
3830
$403
3746
1394
3907
$411
4070
$429
•-TOTAL
55.2
1254,439
$256,432
$258,687
$260,294
$261,477
NON-SLACKS
iSE 2 CHAN8E NUMBER BENEFITS BENEFITS BENEFITS BENEFITS BENEFITS
iROUP
POP
25 ua/dl
CHILDREN
1988
POP
1989
POP
1990
POP
1991
POP
1992
i— 2yr
7277
0.1352
5.3
$20,589
7371
$20,956
7466
$21,227
7475
$21,252
7484
$21,278
2-3
3734
0.1452
7.6
$29,725
9828
$30,012
9960
$30,415
9970
$30,445
9979
$30,473
i-5
9110
0.1202
5.9
$23,023
9167
$23,167
9223
$23,308
9308
$23,523
9356
$23,644
j-7
8486
0.0652
3.0
$11,616
8505
$11,642
8514
$11,655
8647
111,837
8757
$11,987
9-9
7862
0.0002
0.0
$0
7844
$0
7796
$0
7985
$0
8146
$0
10-11
7239
0.0002
0.0
$0
7182
$0
7088
$0
7308
$0
7529
$0
12-13
6615
0.0002
0.0
$0
6521
$0
6379
$0
6653
$0
8930
$0
i-TOTAL
[Al
21.8
. .87.0
$85,053
$339,492
$85,778
$342,210
$86,605
$345,292
$87,058
$347,351
187,383
$348,859
-------
probability 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 larger
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 faie
the same reductions as low lead individuals, reducing the
probablity of falling below 25 pg and biasing down the benefit
est imates.
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. ASES 40-59
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 NHANES II data
by CDC- and EPA personnel, a number of investigations reported a
statistically significant relationship between low to moderate
blood lead levels and blood pressure in males. In addition to
epidemiological analyses, animal studies also demonstrate this
link.'*'7" The research also indicates possible causal pathways by
which lead acts on the cardiovascular system. "*hese 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
fcoxin 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.
^8 Ibid.. pp.M-G - V-15.
-------
the Frarningham 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.4* Since blood
pressure seems to increase with blood lead, so too will the
i nci dene e o f 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
it measures effects at lower water lead c ',:ic ent r at i ons. His
findings are summarized in the following equation:
PbB = a + .OSPbW
wher e:
PbB = blood lead in jjg/dl
a = constant plus other demographic and
environmental factors, and
PbW = water lead in pg/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 (.06 :£ 22.2 pg/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.. pp.V-23 - V-31.
-------
Hyper tension
Medical authorities consider adults having diastolic blood
pressure greater than 90 to be hypertensiye. 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.®0
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 (. 1385) , which
estimates the probability that an adult male will be
hypertensive, performs poorly at b1 nod lead levels <10 jjg/dl .
Consequent 1y, 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.
Cafdiovascular Disease
Having previously estimated the reduction in blood lead
resulting from reduced lead levels in drinking water, calculating
50 Ibid.. p. V—28.
-------
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 (i.e.
8.25 pg/dl and 6.92 pg/dl) in the NHANES 11 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.(See table III)
Myocardial Infarctions. In this analysis, the benefit estimate
for Myocardial Infarctions
-------
TABLE III
ADULT BENEFITS
PARAMETERS
serum cholesterol 213
average age SO
•-^sel me blood pb 17.4
alood pb reduction 1.33
percent applicable 547.
AVOIDED MYOCARDIAL INFARCTIONS
PARAMETERS
avoided cost per MI $65,600
smoking 0.8
1988 1989 1990 1991 1992
start blood lead
8.25
8.23
8.22
8.20
8.19
end blood lead
6.92
6.90
6.89
6.37
6.86
start blood pressure
81.53
81.51
81.51
81.50
31.49
end blood pressure
80.72
30.70
80.70
30.68
30.68
start prob MI
0.00658
0.00658
0.00658
0.00658
0.00S57
end prob MI
0.00643
0.00643
0.00643
0.00642
0.00642
Di f prob MI
0.00015
0.00015
0.00015
0.00015
0.00015
population
36100
36800
37500
33800
40250
avoided Mis
2.95
3.01
3.07
3. 19
*"7 1
-------
TABLE IllCcont.)
AVOIDED DEATHS
PARAMETERS
ivoided cost per death $1,000,000
imoking 2.24
1388 1989 1990 1991 1992
start blood lead
3.25
8.23
8.22
3.20
3. 19
end blood leaa
S. 92
5.90
6.39
S. 37
S. 36
stare blood pressure
81.53
31. Si
31.51
81.30
31.49
end blood pressure
80.72
30.70
30.70
30.63
30.58
start prob death
0.01314
0.01314
0.01314
0.01313
0.01313
end prob death
0.01282
0.01231
0.01281
0.01281
0.01231
Di f prob death
0.00032
0.00032
0.00032
0.00032
0.00032
population
36100
36800
37500
3S800
40250
avoided Mis
6. «i3
6. 42
6.55
6. 79
7.05
benefits
$6,278,613
$6,418,852
$6,547,245
$6,787,263
$7,047,689
TOTAL CVD
$6,586,665
$6,733,774
$6,868,462
$7,120,247
$7,393,446
-------
1980, increasing to 3.3 in 1992. In monetary terms, we valued an
MI at $65,600, yielding total annual benefits avoided Mis at
*5193,000 in 1988, rising to *217,000 in 1992."
Strokes. Strokes are a debilitating form of cardio-vascular
disease that can leave parts of the central nervous system
permanently damaged. In est i mat i ng the benefits achieved from
avoided strokes, the analysis includes only medical costs and
foregone wages.
The estimation procedure uses the Fr amingham study risk
regression equation assessing the probability of suffering a
stroke based on systolic blood pressure, age, smoking behavior
and serum cholesterol."3 Using the same procedure employed for
Mis, we estimated that 1.75 strokes can be avoided, rising to
1.96 in 1992; at $49,000 per stroke, this produces benefits of
$115,000 *n 1988 and $129,000 in 1992.®'*
Death*. In addition to assessing risks for strokes, the
Framingham 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.9a
52 Ibid.. ~. V—38 -V-39.
53 Ibid.. p. V—31.
54 Ibid.« p.V—40.
55 Ibid.. p. V-31.
-------
Again using the blood pressure calculations from above, we
substituted the blood pressure values into the risk regression
equation to calculate the change in probabi1ity. 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 always 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 $6,300,000,
increasing to *7,000,000 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 $6,600,000 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 Franungham 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 effects
-------
of age 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 monetised 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
-------
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
overwhel mi ngly 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
r esul t 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
-------
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 solder 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 -?.re also hampered by the lack of direct measures of
corrosion rates for Boston. Consequent 1y, 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 $22.68/capita in 1985 dollars.®®
Furthermore, the National Bureau of Standards believed that
corrosion control techniques used in the 1970s could reduce the
costs of materials damage by 20"/.. Based on this judgement, the
avoidable per capita cost is $4.53.
56 Ryder, Journal of the American Water Works Association, May
1980, p.283.
-------
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.®'5'
Applying this incremental improvement to the savings already
achieved, we can expect an additional $1.13/capi ta reduction in
materials damage annually from the new treatment or $635,000 for
the city.
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 15% to 50%.®" Using the
Region I data and assuming the prescribed treatment will maximise
corrosion control, the 'effectiveness of control will increase
from 75% to 90%. Assuming a linear relationship between
corrosion control and reduced materials damage, this 15%
improvement in control will result in a 9.757. reduction in
materi als damage or $2.21/capita annually C.0975 $22.68).
Total cost reduction in Boston would therefore be $1,242,000, By
averaging the two estimates we arrive at a benefit figure of
¦$939,000 annually for reduced materials damage.
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 rng/L which
represents an additional 25% improvement.
38 AWWA, oo.c i t. . p. 590.
-------
38
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 $1,500,000. Because all MWRA consumers would reap
the benefits of additional treatment, it is reasonable to
apportion costs to Boston based on its consumption.'9'® According
to the MWRA demand projections, Boston consumes 43% 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 $45,000.
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, Mater demand projections.
Prepared by Wallace, Floyd, Associates Inc., January 1983, p. IS.
-------
37
With respect to 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 $8,700,000 in 1992 (see 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 $7,200,000 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 $1,300,000 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
$500,000 in 1988.
Since our calculations involve a number of stages (i.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
out comes. 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 highest
b en e f i t s.
For our optimistic alternative, we used the AWWA
treatment cost estimate. Driven by lower chemical costs,
-------
TABLE IV
TOTAL BENEFITS
1988 1289 1990 1991 1992
children $339,492 $342,210 $345,292 *347,351 $348,359
myocardial infarctions $193,410 $197,728 $201,682 $209,074 $217,096
strokes $114,642 $117,194 $119,534 $123,910 $128,661
deaths $6,273,613 $6,418,352 $6,547,245 $6,737,263 $7,047,689
materials damage $939,000 $939.000 $939.000 $939,000 $939.000
total w/o CVD $1,278,492 $1,281,210 $1,284,292 $1,286,351 $1,237,859
total *7,865,157 $8,014,983 $8,152,753 $8,406,599 $8,681,305
-------
TABLE V
COST BENEFIT CQMPARISIQN
1988
1989
1990
1991
130;
net total
b/c ratio
$7,179,176 $7,329,003 $7,466,773 »7,720,618 '$7,995,324
11.S 11.7 11.9 12.3 12.7
net w/o CVD
b/c ratio w/o CVD
$592,511 $595,229 $598,311 $600,371 $601,878
1.9 1.9 1.9 1.9 1.9
-------
Boston's share of annual treatment cost would be "8550,000. To
calculate benefits we used the following assumptions: apply water
lead data to 70'/. of the population; use the high 95"/. 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 1988, rising to $12,775,000 in 1992 (see table VI H.
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 $850,000. 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 1ow 95% confidence interval for water lead
reduction - .018 rng/L; and the low estimate for materials damage
- $635,000. This scenario yielded $3,950,000 in annual net
benefits for Boston in 1988, rising to $4,330,000 in 1992 (see
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 characterised 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
1988
1989
1990
1991
1992
cm i or en
myocardial infarctions
strokes
deaths
materials damage
$495,375
$302,508
$179,239
§499,544
$309,279
$183,238
$5u4,^64
$315,470
$186,901
$507,002
$327,045
$193,749
$509,003
$339,599
?201,181
$9,320,761 $10,040,666 $10,241,690' $10,617,533 $11,025,123
$1.242.000 $1.242.000 $1.242.000 $1.242.000 $1.242.000
total
*12,033,883 $12,274,726 *12,490,325 *12,887,329 *13,316,911
COST BENEFIT CQMPARISIQN
1988 1989 1990 1991 1992
net total
b/c ratio
$11,499,866 $11,734,709 $11,950,303 $12,347 77o, 833
17. £ 17.3 18,2 18,3 19.4
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TABLE VII
TOTAL BENEFITS
i3sa
1989
1990
chiIdren
Myocardial infarctions
strokes
a&aths
materials damage
total
§180,096
5114,594
$67,951
$3,719,837
$635.000
$181,639
$117,146
$69,459
$3,802,728
$635.000
$183,401
$119,487
$70,346
$3,878,725
$635.000
$184,343
$123,862
$73,43£
$4,020,773
$635,000
$185,021
$128,612
$76,251
$4,174,982
$635.000 $635.000 $635.000 $635.000 $635.000
*4,717,477 $4,805,373 *4,887,459 *5,037,419 *5,199,866
COST BENEFIT COMPARISION
1988 1989 1990 1991 1992
net total
b/c ratio
$3,848,092 $3,936,587 $4,018,073 $4,168,034 $4,330,480
S. 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
ot her c ommuni t i es.
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 or thophosphate, 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.
Consequent 1 y, 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 benefi:s.
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40
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 to 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 treatment 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) Consequent 1y,
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«s types and extent of
materials found in its distribution system. Communities must
also institute a comprehensive monitoring pi an 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.
•Cru. S. GOVERNMENT PRINTING OFFICE I 1 98 8-S I S-0 0 2/8 0 1 5 0
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