vvEPA
               United States
               Environmental Protection
               Agency
               Office of Policy
               Planning and Evaluation
               Washington DC 20460
Reducing Lead
in  Drinking Water:
A  Benefit Analysis
December 1986
Draft Final Report
EPA-230-09-86-019

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

             Draft  Final Report
               December 1986
             U,5. Environmental Pretcctwn
             rtegion 5, Library (PL-12J)
             77 West Jackson Boulevard, 12th Fta*
             Chicago, II  60604-3590

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                             SUMMARY


     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)

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

intended to protect against known or anticipated adverse health

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

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

includes cost and technological constraints.   MCLs are proposed

at the same time as the MCLGs.

     On November 13, 1985, EPA proposed National Primary Drinking

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

chemicals,  11 inorganic chemicals,  and 4 microbiological parameters
*  Defined in the Act as water systems serving 25 or more people
   or having at least 15 service connections.

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in drinking water; these substances are listed in Table 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.


A.  Summary of Study

     This analysis estimates some of the benefits that could result

from reducing exposure to lead in community drinking water supplies.

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

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

B.  Inorganic Chemicals

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

C.  Microbiological Parameters

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

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and reduced materials, damages relating to the phenomenon of lead's

presence in drinking water — as a corrosion by-product.  In addi-

tion, because the calculation of health benefits depends on the

extent of human exposure, another section 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 main-

taining the current high guality 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.*

     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.
 *   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.

 **  The 1986 Economic Report of the President to Congress {Table B-4)

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1.  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 distri-

bution and residential plumbing systems (cf sources as diverse

as the EPA Air Quality Criteria Document for Lead, 1986; Craun

and McCabe, 1975; Kuch and Wagner, 1983; Lead in (British) Drinking

Water, 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 can be much higher than those found at the treatment

plant.  While the presence of lead service pipes and mains is

relatively restricted geographically 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 house-

holds 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 l-iving in new housing, or in older

housing but with new plumbing, are especially at risk of high

levels of lead in the drinking water (Sharrett et al., 1982;

Murrell, 1985).  In general, lead concentrations in fully flushed

water typical of distribution system water, even under corrosive
*   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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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 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;* 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 compli-

ance with EPA's monitoring regulations.  The Culligan 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

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., 1982; Internal Corrosion of Water
*  The use of company names and the presentation of related data
   does not constitute endorsement of their services.

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 Distribution  Systems,  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.,

 1982;  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) indicates  that the average

.household  contains 2.73 individuals  (Table 58).  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

 8 percent** of new plumbing is plastic, so 92 percent  of the
 *    Survey of Current Business,  U.S.  Department of Commerce -
     Bureau of Economic Analysis,  1985;  Table on New Housing
     Construction.

 **  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).

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                                8


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

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

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

     To calculate the risk to inhabitants of older housing,  subtract

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

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

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

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

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

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

exposure estimates indicated that 41.8 million people using public

water supplies currently may be exposed to some water that exceeds

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

     This may be a low estimate

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

        0  because we have not included those who, while living
           in older housing, have recently had major plumbing
           repairs and so are also at risk of the potentially high
           lead levels associated with newly installed solder;

        0  because the Culligan data represent water that is
           harder than average, whereas high lead levels are
           often found with soft waters; and
                          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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        0  because the data used are for partially flushed
           samples,  while some people (especially children)
           may consume water that is closer to first-flush
           or standing samples (which is more likely to
           contain higher concentrations of lead).*

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

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

community water supplies.

     There are uncertainties, however, concerning actual patterns

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

construction that  would 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 (1986).  Those

documents assume a linear relationship, at least at the lower blood

lead levels typical of the United States, with different constants

for children and adults.  Those formulae are:

     (for children)t pbB** = 0.16*** x intake of lead from water

     (for adults)  PbB** = 0.06*** x intake of lead from water.
*   Water standing in pipes has a greater opportunity for lead to
    leach into it and, therefore, is more likely to contain higher
    lead levels.

**  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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                                 10
 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 on 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-institutionalized




 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., 1980 and  1982; Mahaffey et al. , 1982; Pirkle and



 Annest, 1984).






 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:



 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 (1986),  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 bio-

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                                  11
  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



  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-
  *   ALA,  or  aminolevulinic  acid.

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                                12






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




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  10 point decrement.  These esti-




mates neither include many  major  categories of pathophysiological

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                                13


effects (e.g., renal damage), nor do either the medical costs

or the compensatory educatio-n costs consider any lasting damage
          •
no.t 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 the 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

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

estimate the effect of 10 point losses that can occur as a part of

the cognitive damage caused by lead exposure upon expected future

earnings: one 10 point can directly and indirectly affect earnings

by 0.9 percent.  The studies of cognitive damage presented in

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                                14


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,

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.**
*  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.

** This also biases the results downward because there is a strong
   rationale for considering these effects as additive.

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                                15





     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.





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
   Statistical Abstracts (1986), Tables 27 and 82.

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                               16


(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 b.lood 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 MHANES

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  (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
* 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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                                 17






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




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.

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                                 18






     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).




     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,  1984), 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

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                                 19






 $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.






 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 the most part,  therefore,  treatment



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.

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                                20


     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 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 Boston and Seattle, cities currently treating their

highly corrosive waters) to almost $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 treat-

ment 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

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
*  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

** Of the total population of about 240 million, 219.2 million
   people are served by community water systems.

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                                                               21
TABLE 2.  Estimates of Annual Per Capita Corrosion Damage (1985 dollars)
Studies
Kennedy Engineers
(1973)
Hudson & Gilcreas
(1976)
Kennedy Engineers
(1978)
Bennett et al.
(1979)
(cited in Ryder,
1980)
Energy & Environ-
mental Analysis
(1979)
Ryder (1980)
Kirmeyer & Logsdon
(1983)

Estimated Annual Corrosion Damage
(per capita)
Distribution
Systems
$5.57
$8.68*
—
$9.40
$3.98
$1.17
L

Residential
—

$30.87*
—
$7.97
$22.19
$23.60*

Total
$16.71*.
$26.04*
$46.30*
$28.20*
$11.95
$23.36
$35.40*

Corrosion
Damage
Avoidable
Through
Water
Treatment
30%*
50%
20%
20%
38%
25%
40%

Annual Per
Capita Benefits
of Corrosion
Control
$5.01*
$13.02*
$9.26*
$5.64*
$4.54
$5.84
$14.16*
AVERAGE $8.21
W/OUT EEA $8.82
Assumpt ions/Notes
Assumed 30% potential reduction
in corrosion damage and that dis-
tribution costs were one-third of
total costs.
They did not include increased
operating costs. Per capita
estimate assumes 200 million
people are served by public water
systems. Assumed that distri-
bution costs were one-third of
total costs.
They calculated $6.17 per capita
in savings to residence owners.
Assumed residential costs were
two- thirds of total costs.
Assumed that 200 million people
are served by public water systems
and that distribution costs were
one- third of total costs.
This is an admitted underestimate:
it includes only damage to pipes
(not damage to water heaters,
increased operating costs, etc.)
Ryder ascribed 95% of corrosion
damage to private owners.
Assumed residential costs were
two- thirds of total damage.

      These estimates have been calculated  by the  authors of this  paper.   Assumptions  are  noted  above.

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                                 22
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).


5.    Summary of 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 3, and the non-monetized

benefits are presented in Table 4.

     Based upon the latest cost "estimates used by the Office of

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

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

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

     It should be emphasized that considerable uncertainty is

associated with these estimated benefits, uncertainties derived

both from the current state of knowledge concerning lead health

effects and the valuation of avoiding such effects.  Other

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.
*  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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                                      23
TABLE 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 fron fewer heart attacks
      (white males, aged 40-59)

     -savings from fewer strpkes
      (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 conmunity water systems:   219 million

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

   - children at risk of stature decrement

   - fetuses at risk

   - increased risk of hematological effects
Reductions in Nunfoers
  of People at Risk

  42 million*
     29,000

    230,000
     11,000
        100

     29,000

     82,000

    680,000

     82,40.0
Adult health benefits

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

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

     -strokes
      (white males, aged 40-59)

     -deaths
      (white males, aged 40-59)

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

     -reduced risk of reproductive effects
      (women, aged 15-44)
    130,000


        240


         80


        240


    680,000)
           )
           )

     34,000
* Total population served by community water systems:  219 million

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                                 25
B.   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.*  That analysis, carried out as a



masters thesis project at Harvard University, focused on Boston as



a city with high potential for increased lead exposure via drinking



water.



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



(pH = 6.7) and soft (14 mg/1 of 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.,  1975; and several internal studies conducted by the



Massachusetts Water Resources Authority and the [Boston]



Metropolitan District Commission).



     To reduce the high lead levels, 'Boston began corrosion



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



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



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



concentrations generally decreased to below the current MCL of



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



a lowered MCL.



     Jacobson analyzed the incremental annual costs and benefits



of additional efforts by Boston to control further the corrosivity
* He assumed a lowered MCL of 10 ug/1 because that is the

  feasibility limit for current treatment and technology.

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                                26


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;

        0  it will be impossible for every tap to meet the lowered
           MCL, even using state-of-the-art treatment,  and so
           samples should be averaged; and

           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 (1985).

     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
* 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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                                27
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 unclear, however, 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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                            REFERENCES
American Water Works Association. Water Quality Division Committee
  report. Determining internal corrosion potential in water supply
  systems. JAWWA 1984 August'? p. 85-88.

American Water Works Association.  Internal corrosion of water
  distribution systems. Comparative research report. 1985.

Anderson R, Berry D. Regulating corrosive water. Water Resources
  Research. 1981 December; 17(6):  1571-1577.

Angle CR, Mclntire MS.  Children, the barometer of environmental
  lead. In:  Harness L (ed):  Advances in Pediatrics, Yearbook
  Medical Publishers, Inc., Chicago 1982; pp 3-32.

Angle CR, Mclntire MS, Swanson MS, Stohs SJ. Erythrocyte
  nucleotides in children - increased blood lead and
•  cytidine triphosphate.. Pediatric Research 1982; 16: 331-4.

Annest JL, Mahaffey KR, Cos DH, et al. Blood lead levels for
  persons 6 months - 74 years of age:  United States 1976-1980.
  National Center for Health Statistics, Advanced Data no. 79,
  May 12, 1982.

Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG.
  Chronological trends in blood lead levels between 1976 and
  1980. New England Journal of Medicine 1983; 308: 1373-7."
                                                          *
Bellinger D, Needleman H, Leviton A, Waternaux C, Rabinowitz M,
  Nichols M. Early sensory-motor development and prenatal exposure
  to lead. Neurobehavioral Toxicology and Teratology 1984;
  6:387-402.

Bellinger D, Leviton A, Waternaux C, Needleman H, Rabinowitz M.
  A longitudinal study of the developmental toxicity of low-level
  lead exposure in the prenatal and early postnatal periods. Paper
  presented at the Heavy Metals in the Environment Conference,
  Athens, Greece. 1985.

Bellinger D, et al. Correlates of low-level lead exposure in
  urban children at 2 years of age. Pediatrics 1986 - in press.

Bornschein RL. "Effects of prenatal and postnatal lead exposure
  on fetal maturation and postnatal growth", to be presented
  at the Joint EPA-EEC conference on Lead and Neurotoxicity,
  Edinburgh, Scotland. September 1986.

Britton A, Richards WN.   Factors influencing plumbosolvency.
  Journal of the Institute of Water Engineers and Scientists.
  1981 July.

-------
Comstock GW. Water quality and cardiovascular disease: a review
  of recent studies in Canada and the US.  Paper presented at the
  International Symposium on Geochemistry and Health, London,
  England; April 1985.

Craun GF,  McCabe LG. Problems associated with metals in drinking
  water. JAWWA 1975 November; 67(11):593.

Dangel RA. Study of corrosion products in the Seattle water
  department distribution system, U.S. EPA report 670/2-75-036.
  Cincinnati, Ohio.  1975.

De la Burde B, Choate MS Jr. Does asymptomatic lead exposure in
  children have latent seguelae. Journal of Pediatrics 1972;
  81: 1088-91.

De la Burde B, Choate MS Jr. Early asymptomatic lead exposure
  and development at school age. Journal of Pediatrics 1975;
  87: 638-42. '

Dietrich KN, Kraft KM, Shukla R, Bornschein RL, Succop PA.
  The neurobehavioral effects of prenatal and early postnatal
  lead exposure. In Schroeder (ed): Mental Retardation, Neuro-
  behavioral Toxicology and Teratology,  1986 - in' press.

Durfor CN, Becker E. Chemical quality of public water supplies .
  of the U.S. and Puerto Rico, 1962. Hydrologic Investigations
  Atlas HA-200. U.S. Geological Survey.  1964a.

Durfor CN, Becker E. Public water supplies of the 100 largest
  cities in the U.S., 1962. Geological Survey Water-Supply Paper
  1812. U.S. GPO, 1964b.

Energy and Environmental Analysis. Health and corrosion impact of
  soft water. Prepared for the A/C Pipe  Producers Association.
  1979 August.

Erickson MM, Poklis A, Gantner GE, Dickinson AW, Hillman  LS.
  Tissue mineral levels in victims of sudden infant death syndrome
  I.  toxic metals - lead and cadmium. Pediatric Research 1983;
  17: 784-99.

Harlan WR, Landis JR, Schmouder RL, et al. Relationship of
  blood lead and blood pressure in the adolescent and adult
  U.S. population. Journal of the American Medical Association,
  1985 January 25.

Hartunian NS, Smart CN, Thompson MS.  The Incidence and Economic
  Costs of Major Health Impairments.  Lexington, MA:   Lexington
  Books 1981.

-------
Hudson HE Jr, Gilcreas FW. Health and economic aspects of water
  hardness and corrosiveness.  JAWWA 1976; 68:  201-204.

ICF. A survey of the literature regarding the relationship between
  measures of IQ and income. Prepared for U.S. EPA, Office of
  Policy Analysis, 1984.

Internal Corrosion of Water Distribution Systems. Report of the
  AWWA Research Foundation and the DVGW - Forschungstelle. 1985.

Jacobson J.  The costs and benefits of reducing lead in Boston's
  water.  Masters thesis submitted to Harvard University, Kennedy
  School of Government, Spring 1986.

Kakalik JS, et al. The Cost of Special Education. Rand Corporation
  Report N-1791-ED, 1981.

Karalekas PC, Craun GF, Hammonds AF, Ryan CR, Worth DJ.  Lead and
  other trace metals in drinking water in the Boston metropolitan
  area.  Proceedings of the 1975 AWWA Annual Conference, Minneapolis,
  MN.

Karalekas PC, Ryan CR, Larson CD, Taylor FB.  Alternative methods
  for controlling the corrosion of lead pipe.  Journal of the New
  England Water Works Association 1978 June.

Karalekas PC, Ryan CR, Taylor FB. Control of lead pipe corrosion
  in the Boston metropolitan area. Proceedings of the 1982 AWWA
  Annual Conference, Miami Beach, Florida.

Karalekas PC, Ryan CR, Taylor FB. Control of lead, copper, and
  iron pipe corrosion in Boston, JAWWA. 1983 February.

Karalekas PC. Impact of lead piping and fittings on drinking
  water quality. Proceedings of a Seminar on Plumbing Materials
  and Drinking Water Quality.  Sponsored by US EPA; Cincinnati,
  Ohio; 1984 May.

Kennedy Engineers. Internal corrosion study, summary report.
  Conducted for the city of Seattle, Washington; 1978 February.

Kirmeyer GJ, Logsdon GS. Principles of internal corrosion and
  corrosion monitoring. JAWWA 1983 February; pp. 78-83.

Kuch A, Wagner I. A mass transfer model to describe lead con-
  centrations in drinking water. Water Research 1983; 17 (10):
  1303-1307.

Lassovszky P. Effect on water quality from lead and nonlead solders
  in piping. Heating/Piping/Air Conditioning, 1984 October; pp. 51-58

Lead in Drinking Water: A Survey in Great Britain. Pollution
  Paper 12.  Dept. of the Environment HMSO, London, 1977.

-------
Levy RI.  The decline in coronary heart disease mortality: Status
  and perspective on the role of cholesterol. American Journal
  of Cardiology 1984 August 27;  54 (4).

Mahaffey KR, Annest JL, Roberts  J, Murphy MS. National estimation
  of blood lead levels: United States (1976-1980). New England
  Journal of Medicine 1982; 307: 573-9.

McGee D,  Gordon T.  The results  of the Framingham Study applied to
  four other U.S. - based epidemeologic studies of coronary heart
  disease.  The Farmingham Study.  Section 31.  DHEW Pub No.  (NIH)
  76-1083.  National Institutes  of Health, Washington, D.C. U.S.
  Government Printing Office 1976.

Midwest Research Institute. Occurrence and impacts of aggressive
  water systems. MRI publication. 1979.

Millette JR, Hammonds AF, Pansinq MF, Hanson EC, Clark PJ.
  Aggressive water:  assessing the extent of the problem.
  JAWWA 1980; 72 (5):  262-66.

Moore MR, et al. Some studies of maternal and infant lead exposure
  in Glascow. Scotish Medical Journal 1982; 27: 113-122.

Mruksa.  Plastic piping and joining materials.  Presented at:
  Plumbing Materials and Drinking Water Quality Seminar? sponsored
  .by EPA; Cincinnati, Ohio; 1984.

Multiple Risk Factor Intervention Trial:  Risk  factor changes and
  mortali'ty results. Multiple Risk Factor Intervention Trial
  Research Group. JAMA 1982? 248: 1465-77.

Murrell NE. Impact of metallic solders on water quality.  Presented
  at the Specialty Conference on  Environmental  Engineering, Ameri-
  can Society of Corrosion Engineers. Boston 1985.

National Center  for Health Statistics.  Plan and Operation  of the
  Second National Health and Nutrition Examination Survey 1976-
  1980.  National Center for Health Statistics  1981  (Vital  and
  Health Statistics Series 1, No. 15).

Nielsen K. Contamination of drinking water by cadmium and  lead
  from fittings. Danish Building  Research Institute. 1975.

Nielsen K. Dissolution of materials from  service  pipes and  house
  installations  and  its sanitary  aspects. International  Water
  Supply Association.  Amsterdam  Conference;  1976.

Nielsen K. Corrosion of soldered  and brazed  joints  in tap  water.
  British Corrosion Journal  1984;  19(2):  57-63.

Oliphant R.  Lead  contamination  of potable water arising  from
  soldered  joints.   Water  Research Centre Report  #125E.
  England;  1983.

-------
Patterson JW, O'Brien JE. Control of lead corrosion. JAWWA 1979
  May; 71(5): 264-271.

Patterson JW. Corrosion in water distribution systems. Prepared
  for U.S. EPA, Office of Drinking Water. 1981 March.

Piomelli S, Seaman C, Zullow D, Curran A, Davidow B. Metabolic
  evidence of lead toxicity in "normal" urban children. Clinic Res
  1977; 25: 459A.

Piomelli S, Seaman C, Zullow D, Curran A, Davidow B. Threshold for
  lead damage to heme synthesis in urban children. Proceeding of
  the National Academy of Sciences in 1982 May; 79: 3335-9.

Piomelli S, Rosen JF, Chisolm JJ, Graef JW. Management of child-
  hood lead poisoning. Journal of Pediatrics 1984; 4:105.

Pirkle JL, Annest JL. Blood lead levels 1976-1980 - Reply (letter),
  N Eng J Med 1984; 310(17): 1125-6.

Pirkle JL, Schwartz J, Landis JR, Harlan WR.. The relationship
  between blood lead levels and blood pressure and its cardiovas-
  cular' risk implications. American Journal of Epidemiology, 1985;
  121(2):  246-58.

Pocock SJ, Shaper AG, Ashby D, Delves T, Whitehead TP. Blood
  lead concentration, blood pressure, and renal function.
  British Medical Journal 1984; 289: 872-874.

Pocock SJ, Shaper AG, Ashby D, Delves T. Blood lead and blood
  pressure in middle-aged men. In: Lekkas TD (ed), International
  Conference on Heavy Metals in the Environment. September 1985;
  Athens, Greece.

The Pooling Project Research Group. Relationship of blood pres-
  sure, serum cholesterol, smoking habit, relative weight and ECG
  abnormalities to incidence of major coronary events:  Final
  report of the pooling project. J Chron Dis 1978; 31:  201-306.

Provenzano G. The social costs of excessive lead-exposure during
  childhood. HL Needleman ED. Low Level Lead Exposure;  The
  Clinical Implications of Current Research. New York: Raven
  Press 1980.

Public Use Data Tape Documentation, Hematology and Biochemistry.
  Second National Health and Nutrition Examination Survey 19\76-
  1980. Catalog number 5411, U.S.  Public Health Service, National
  Center for Health Statistics.

Richards WN, Moore MR. Plumbosolvency in Scotland - the problem,
  remedial action taken and health benefits observed. JAWWA
  1982 May; p.  901-918.

-------
 Richards WN, Moore MR.  Lead hazard controlled  in  Scotish  water
   systems.  JAWWA 1984  August; p. 60-67.

 Ryder  RR. The costs of  internal corrosion  in water  systems.
   JAWWA 1980 May; pp. 267-279.

 Ryu JE, Ziegler EE, Nelson SE, Fomon  SJ. Dietary  intake of  lead  and
   blood lead concentration in early infancy. Am.  J.  Dis.  Child.
   1983; 137:886-891.

 Schwartz J, Angle C, Pitcher H. The relationship  between  child-
   hood blood lead levels and stature.  Pediatrics  1986; 77:  281-288.

 Schwartz J, Leggett J,  Ostro B, Pitcher  H,  Levin  R.  Costs and
   benefits of reducing  lead in gasoline. U.S.  EPA,  Office of
   Policy Analysis 1985.

 Sharrett AR, Carter AP, Orheim RM, Feinleib M.  Daily intake of lead,
   cadmium, copper and zinc from drinking water:   the Seattle  study
   of trace metal exposure.  Environmental  Research  1982;  p. 456-475.

 U.S. Environmental Protection Agency,  Environmental.Criteria  and
   Assessment Office. Air Quality Criteria  for  Lead.  1986  March.

 U.S. Environmental Protection Agency.  Regulatory  Impact Analysis
   Guidelines.  1984.

-Wibberly DG, Khera AK,  Edwards JH, Rushton  DI.  Lead  levels  in human
   placentae from normal and malformed  births.  Journal of  Medical
   Genetics 1977; 14: 339.

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