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OCR for page 243
The Health Effects of
Environmental Lead Exposure:
Closing Pandora's Box
Deborah C. Rice
Lead has been recognized as a poison from ancient times to the
present (Cantarow and Trumper, 1944; Oliver, 1914~. Over the last
decade or so, attention has focused on the subtle effects of environ-
mental exposure at levels presently considered "normal" in our in-
dustrialized age [Landsdown and Yule, 1986; Mahaffey, 1985; Na-
tional Academy of Sciences (NAS), 1980; Needleman, 1980; Rutter
and Russell Jones, 1983~. The resultant research has inspired lively
and sometimes heated debate concerning the nature and possible threshold
of these effects. The recognition that lead produces intellectual im-
pairment in children, as well as other health effects, has resulted in
the progressive tightening of regulation of lead in the United States
and other countries, including the phaseout of lead from gasoline
[Environmental Protection Agency (EPA), 1984; see Johnson and Mason,
1984, for review of U.S. lead regulations].
Exploration over the last decade of the effects of environmental
exposure to lead, neuropsychological and otherwise, represents a case
study in the scientific and political procedures, problems, and fail-
ures inherent in such an endeavor. As such it can be used as a model
for discussion in light of the theme of Part III of this volume chemi-
cal time bombs. All individuals in industrialized societies carry a
significant body burden of lead, a situation that will take at least a
generation to change even if lead were removed from the environment
instantaneously tomorrow. What have been, and what can we antici-
pate will be, the consequences of this mass exposure? What are the
243
OCR for page 244
244
DEBORAH C. RICE
issues critical to this evaluation, and what should be clone differently
in the future?
HISTORY OF THE PRESENT PERSPECTIVE ON THE
ENVIRONMENTAL NEUROTOXICITY OF LEAD
Although legal is a common element in the earth's crust, its ubiqui-
tous presence in bioavailable forms in the environment is due largely
to the activities of humans (see Lin-Fu, 1985; Smith, 1986 for reviews).
Lead has been used in metalworking and in pottery glazes for mil-
lennia. The Romans used lead for plumbing as well as a sweetening
agent in wine and other foods. The industrial revolution and the
addition of lead to gasoline in the 1920s have resulted in dramatic
increases in environmental lead levels (Elias et al., 1975~. Present
blood levels of industrial populations are highly correlated with the
amount of leader} gasoline in use (Hunter, 1986~. Present environmental
levels are several orders of magnitude above preindustrial levels (NAS,
1980; see Table 1~. The bodily burden of lead in human bones is pres-
ently 500-foIct greater than in prehistoric times, and the present diet
of Americans contains 100 times more lead than prehistoric diets
(NAS, 1980~.
The inclusion of tetraethyllead as a gasoline aclctitive in the 1920s
was a lan~lmark event that resulted in a steep increase in lead emit-
ted into the environment (Elias et al., 1975~. The overtly toxic effects
of lead were already recognized at that time; the use of lead as a
TABLE 1 Comparison of Estimated Natural Levels of Lead in the
Environment with Typical Present-Day Levels
Natural Present Approximate Ratio,
Medium Concentration Concentration Present/Natural
Air
Rural/remote 0.01-0.1 ng/m3 0.1-100 ng/m3 10-1,000
Inhabited 0.1-1.0 ng/m3 0.1-10 g/m3 100-10,000
Soil
Rural/remote 5-25 g/g 5-50 g/g 1-2
Inhabited 5-25 g/g 1~5,000 g/g 2-200
Water
Fresh
Ocean
Food
0.005-10 g/L
0.001 g/L
0.0001-0.1 g/g 0.01-10 g/g
0.005-10 g/L 1
0.005~.015 g/L 10
100
SOURCE: NAS (1980).
OCR for page 245
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
245
gasoline additive engendered grave warnings by health professionals
concerning the potential threat to the general health as a result of
lead exposure (Rosner and Markowitz, 1985~. This concern was based
on occurrences of mortality and severe neurologic and psychiatric
signs in workers exposed during manufacture of this additive. A
committee convened by the Surgeon General warned in 1926 (in Rosner
and Markowitz, 1985~: "It remains possible that if the use of leaded
gasoline becomes widespread, conditions may arise very different
from those studied by us.... Longer experience may show that even
such slight storage of lead as was observed in these studies may lead
eventually in susceptible individuals to recognizable or to chronic
degenerative diseases of a less obvious character." Despite the rec-
ommendation by the committee that the matter be studied further,
the interests of the automotive and oil industries won out, lead re-
mained in gasoline, and no further data were collected.
In the 1940s, it was recognized by astute physicians that children
who had been treated for lead poisoning suffered permanent sequelae
in the form of neurological damage (Byers and Lord, 1943~. High-
level lead exposure in children at that time was via lead-based paint.
Byers and Lord reported poor school performance, impulsive behav-
ior, short attention span, restlessness, and occasional neurological
signs in these children. These observations were later replicated by
other investigators Jenkins and Mellins, 1957; Perlstein and Attala,
1966; Thurston et al., 1955~.
In the 1970s, concern arose in the United States and elsewhere that
the tons of lead being introduced into the environment every year by
the use of leaded gasoline, as well as other industrial processes, were
producing significant health effects, particularly in children. The
new concern was that common environmental levels of lead were
producing intellectual impairment in children that had no overt signs
of lead poisoning. Early in the decade, attention focused on children
who had ingested lead-based paint (de le Burde and Choate, 1972;
Lin-Fu, 1972~. Deficits in IQ, fine motor performance, and behavioral
disorders such as distractibility and constant need for attention were
observed in children who had never exhibited overt signs of lead
intoxication.
A new understanding of the insidious effects of lead on the intel-
lectual capacity of a large number of children arose with the landmark
study of Needleman et al. in 1979. These investigators reported decreased
IQ and increased incidence of distractibility and inattention in middle-
class children with no exposure to lead from paint. The conclusion
to be drawn from this research was that environmental sources were
responsible for the increased lead burden in these children, and that
OCR for page 246
246
DEBORAH C. RICE
this environmental contamination at levels that had come to be re-
garded as "normal" could be insidiously robbing children in industrialized
countries of their intellectual birthright. Largely as a result of that
study, the last decade has witnessed intense research into the health
effects of lead and the sources of exposure of the general population.
The issue has generated a great deal of political as well as scientific
controversy. Involved have been physicians, epidemiologists, chem-
ists, geologists, animal researchers, representatives of the lead indus-
try, and members of a host of government agencies in a number of
countries. The result of this intense scrutiny is that probably more is
known about the health effects of lead than any other noncarcinogenic
environmental contaminant.
OVERVIEW OF MODERN STUDIES
There have been a number of cross-sectional (retrospective) stud-
ies since 1979 concerning the effects of lead on intellectual and other
behavioral functions in children. The general trend has been to study
children with increasingly lower body burdens of lead and to focus
on middle class rather than disadvantaged children. These studies
have been extensively reviewed (cf. Mahaffey, 1985; Rutter and Russell
Jones, 1983), although new important studies have been published
very recently. There are also several prospective studies going on, in
which the mothers are recruited before the birth of their infants, and
the infants are followed in a longitudinal manner. This design is
stronger than a cross-sectional design, and these studies will undoubtedly
continue to provide important information over the next several years.
This section reviews recently published data from the prospective
studies, as well as the new cross-sectional studies. Alternate meth-
ods of testing for nervous system effects, as well as other recently
reported health effects of lead, are described briefly.
Prospective Studies
Reproductive Effects
It has long been recognized that industrial exposure to high lead
levels produced an increased incidence of miscarriages and stillbirths,
and that infants that did survive failed to thrive and exhibited neuro-
logical abnormalities. Although the situation is less clear for lower
exposure to lead, recent studies provide evidence that low-level lead
exposure causes reproductive problems. Increased maternal blood lead
levels are associated with increased incidence of preterm delivery
(McMichael et al., 1986) and decreased gestational age (Dietrich et
OCR for page 247
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
247
al., 1987; Moore et al., 1982). Blood lead has also been found to be
associated with increased spontaneous abortion (McMichael et al.,
1986~. Higher lead burden may also be associated with minor but
not major physical abnormalities (Needleman et al., 1984), although
this is not a universal finding (Ernhart et al., 1985, 1986; McMichael
et al., 1986~. Increased maternal blood lead level is also associated
with abnormal reflexes, poor muscle tone, and neurological soft signs
such as jitteriness, hypersensitivity, and abnormal cry in the infant
(Ernhart et al., 1985, 1986~. It must be stressed that the maternal and
infant blood lead levels in these studies were in the range considered
normal or average for people in industrialized societies (2-15,ug/dL in
most cases).
It is well established that premature or small-for-date infants are
at greater risk for a variety of behavioral and other health problems.
Such children have more trouble in school and require special help
more often than other children (Schraeger et al., 1966; Weiner et al.,
1968~. Thus, these individuals are likely to represent an ongoing cost
to society over and above any special medical intervention that might
be associated with the neonatal period.
Early Behavioral Effects of Perinatal Lead Exposure
Obviously the functional effects of perinatal lead exposure are not
separate from the effects discussed in the preceding section, but will
in part be related to them. (In fact, controlling for effects such as
gestational age in evaluation of behavioral effects may underestimate
the effects of lead.) There are at least three prospective studies at
present in which women are recruited during pregnancy and the
offspring are monitored at specified ages. In one study by Bellinger
and colleagues (Bellinger et al., 1987a) performance on the Bayley
Mental Development Index (MDI) at 6, 12, and 24 months of age was
associated with cord but not postnatal blood lead levels (Figure 1~.
The difference between the high (mean 14.6,ug/dL) and low (mean 1.8
,ug/dL) blood lead groups was ~7 points. Assessment of these chil-
dren at 57 months of age (Bellinger et al., 1987b) revealed that perfor-
mance on the General Cognitive Index of the McCarthy Scales was
associated with blood lead levels at 24 but not 57 months of age
(after adjusting for possible confounders). Blood levels averaged 6.8
,ug/dL at 24 months and 6.4 ,ug/dL at 57 months.
In the study by Dietrich and colleagues (Dietrich et al., 1987), it
was found that each log unit increment in blood lead was associated
with a covariate-adjusted reduction of 5.7 points on the MDI; the
reduction was 8.0 points if the effects on gestational age and birth
weight were included. One year after birth, prenatal blood lead lev-
OCR for page 248
248
DEBORAH C. RICE
120
a
oh
x
~ ~6
-
c
0, 1
Cal
ID
108
104
Cord Blood Lead Group
~ Low
~ Medium
Hiah
. ~
0 6 12 18 24
Age at Testing (months)
FIGURE 1 Mean Mental Development Index scores at four ages In infants according to
lead level In umbilical cord blood.
SOURCE: Bellinger et al. (1987a).
els were negatively correlated with MDI, Bayley Psychomotor Devel-
opment Index (PDI), and Bayley Infant Behavioral Record (IBR). The
IBR revealed higher activity levels and more negative social-emo-
tional response. In the third prospective study, in Port Pirie, South
Australia (McMichael et al., 1986), a decrease of 2 points in the MDI
scale for every 10 ~g/dL increase in blood lead levels was observed
at 24 months of age. Performance was found to be more related to
postnatal than prenatal blood lead levels; however, no assessment
was performed before 2 years of age. It is possible that early testing
would have revealed significant prenatal exposure effects.
In a retrospective study, Winneke et al. (1985a,b) found that per-
formance on a variety of neurobehavioral and intellectual tasks at 6-
7 years of age was attributable approximately equally to maternal levels
at birth (average 9 ~g/dL) and to current blood levels in the children.
Retrospective Studies on Correlation of l.ead Body Burden
and Behavior in Grade School Children
Since the study by Needleman and colleagues (Needleman et al.,
1979), a number of investigators have examined the effects of moderate-
OCR for page 249
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
20
10
BASC Score
Difference
from School O
Mean
(Adjusted) -1 0
20
_ I I I, I
1.5 2.0 2.5
l
l
3.0 Log Blood Lead
~ ~ 1
10 15 20 25 30
5
249
Blood Lead (pg/dL)
FIGURE 2 British Ability Scales Combined (BASC) score (mean and 95 percent confi-
dence intervals) for groups of children ordered by blood lead.
SOURCE: Fulton et al. (1987).
level exposure on intellectual functioning in children. Such studies
have usually included some measure of intelligence (IQj, school
functioning, teachers' rating of classroom behavior, or specific mea-
sures of attentional mechanisms. Most recent studies have utilized
populations with lower body burdens of lead than the children assessed
by Needleman. For example, Fulton et al. (1987) reported a linear
relationship between intellectual functioning and log blood lead con-
centration for blood lead values between approximately 5 and 25 ,ug/
dL (mean about 10 ,ug/dL) in children living in Edinburgh, with no
indication of a threshold for lead effect (Figure 2~. Results were
significant after adjusting for potential confounders. Another study
of middle-class children in New Zealand (Silva et al., 1988) reported
high correlations between log blood lead (mean 11 ,ug/dL) and mea-
sures of inattention and hyperactivity, after adjusting for confounding
variables. A number of other studies published since 1980 have also
reported a negative association between lead body burden and
performance (Hansen et al. 1987; Hatzakis et al., 1987; Hawk et al.,
1986; Schroeder et al., 1985; Winneke and Kraemer, 1984; Winneke et
al., 1983; Yule et al., 1981), although this finding has not been universal.
(This issue is discussed in a later section.)
Treater Behavioral Concomitants of Increased Lead Burden
The consequences of early poor performance as a result of lead
exposure in terms of grade retention or need for special education
have been little investigated. In a follow-up of children from the
OCR for page 250
250
DEBORAH C RICE
T^BLE 2 Indices of Academic Failure
Dentine Lead Level Academy Aide Grade Retentions
Low 17~ (8/4~ 13~ (2/4~
Midrange 18.6~ (13/70) 11.6~ (8/69)
Elevated 36.4~ (8/22) 22.7~ (5/22)
Total 20.9~ (29/139) 10.9~ (15/138)
(2) = 3.~, ~ < 0.20.
~ ~(2) = 5.61, p < 0.10.
a: I
Needleman et aL (1979) study, BeUinger et aL (1984) reported a Ove-
fold Increase in grade retention and a twofold increase in the need
for academic aid in teenagers' based on tooth lead levels as 5 and 6
year aids (Table 2). Barrett (1978) reported a dose-related increase in
Satisfactory school performance as a function of increased free
erythrocyte protoporphyrin (PEP) levels (a measure of lead expo-
sure). These results are not surprising in view of the effects of lead
on classroom performance in the early grades. Needleman et aL
(1979) reported dose-dependent disordered classroom behavior as
measured by a teacher's rating scale (Figure 3). These results were
replicated by Yule et aL (1981) and Lansdo~n et aL (1983) in Bribsh
children and HatzaHs et aL (1987) ~ Greek children. Yule also reported
that children Fin high lead leveb excited more deviant performance
on tests of conduct problems, inattentive-passive' and hyperactivity
scales. Such early attentional deficits and their associate behaviors
place children at Ask for academic failure and behavior problems
(Uorn and Packard' 1985\ It is hoped that investigators ~1 continue
to follow the children tested initially in the early grades, collecting
data on school performance' special needs, and antisocial behavior.
Effects of Lead on Other Neuropsychologlcal Endpoints
Lead is associated with increased reaction time (Figure 4) and in-
creased errors on various performance tasks (Uat~akis et aL, 1987;
Needleman, 1983; Winneke and Kraemer, 1984; Winneke et aL, 1983,
1985~,b~ Using the Second National Health and Nutrition Examina-
bon Survey (NH^NES D) data base' Schwartz and coUeagues found
an association between lead and increased hearing threshold in chip
dren with blood leveb between 5 and 45 ~g/dL' with no threshold for
OCR for page 251
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OCR for page 252
252
50(3 -
450
-
-
y 400
As
350
300-
Block I Block 11
Delay: as 1 as
DEBORAH C. RICE
Needleman et al.
Yule et al.
High Pb
x= 35 ~g/dL
Low Pb
x= 24 ~g/dL
High Pb
x= 17 ~g/dL
Low Pb
x= 7.4 ~g~dL
Block 111 Block IV
1 as as
FIGURE 4 Performance of children on a simple reaction time task as function of blood
lead levels (K1 = time on task).
SOURCE: Needleman (1987b).
effect (Schwartz and Otto, 1987) (Figure 5), as well as slowed nerve
conduction velocity at blood lead levels above 20-30 ~g/dL (Schwartz
et al., 1988~. Blood lead levels of 15 ~g/dL and below are also asso-
ciated with changes in EEG pattern and auditory evoked potentials
(Otto, 1987; Otto et al., 1981).
Other Health Effects of Environmental Lead Exposure
In addition to effects on the nervous system, low-level exposure to
lead affects a number of important metabolic processes. The most
widely recognized of these are changes in the hematopoietic system.
High intake of lead produces anemia, an effect influenced by iron
status. Lead also inhibits a number of enzymes involved in heme
biosynthesis (see Moore and Goldberg, 1985 for review). The result
is a buildup of some of the precursors involved in heme synthesis.
Inhibition occurs at somewhat different levels for different enzymes,
but some are reliably affected at blood lead values of 10415 ~g/dL, which
are observed routinely in the general population. The buildup of
blood protoporphyrins is the basis of the screening program for un-
OCR for page 253
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
253
due lead exposure of children [Centers for Disease Control (CDC),
1985], because these precursors are easier to measure than blooc! leacl
itself. Aside from frank anemia observed only at relatively high blood
lead levels, the significance of these biochemical changes is in their
potential contribution to lead r~europa~ology and as markers of exposure.
Lead interferes with vitamin D synthesis at low (environmental)
levels (Rosen, 1985~. Such an effect has important health implica-
tions in terms of calcium homeostasis, cell differentiation, and
immunoregulatory capacity. Results from the NHANES II survey
indicate that increased lead burden is associated with decreased stat-
11
10
9
J
I
m
-
o 8
a,
~ 7
ID
ID
° 6
Q
I
A
Cal
A:
4
3
.
2
l
·
.
.
.
.
0 5 10 15 20 25 30 35 40 As
Blood lead level (pg/dL)
FIGURE 5 Relationship of 2-kHz pure tone hearing thresholds and blood lead levels
in 4,519 NHANES II subjects aged 14-19 years.
- SOURCE: Schwartz and Otto (1987).
OCR for page 257
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOS ARE
257
the covariant hypothesis ignores the large body of data from animals,
particularly monkeys, that report behavioral deficits analogous to those
found in children (i.e., deficits in attention and information process-
ing).
Another statement often made by reviewers with respect to the
effects of lead is that they are small, representing only a few percent
of the total variance. However, in general a 10-,ug/dL increase in blood
lead results in about a 4-6 point decrease in intelligence. That degree
of deficit represents 0.30-0.45 standard deviation of the normal dis-
tribution and results in a significant shift of the population. For
example, Needleman (1983) reported cumulative IQs in children with
high and low lead levels for which the mean differed by 6 points.
The resulting distributions revealed that the number of children with
IQs below 80 increased by a factor of four in the high-lead group,
whereas the number of children with IQs over 120 decreased by an
equal amount (Figure 6~. If it is in fact the case that increasing blood
lead levels from 5 to 15 ~g/dL (or from 0 to 10 ,ug/dL) shifts the popu-
lation IQ by approximately 0.4 standard deviation, this represents a
profound and calamitous health effect for any society.
Adequacy of Behavioral Methodology
One problem with the use of intelligence scales is that results are
very heavily environmentally determined. This has often resulted in
the effect of lead apparently decreasing when environmental factors
such as socioeconomic status and scores of home care were included
in the analyses. It therefore would be highly desirable to develop
tests that were less environmentally influenced. Tests such as vigi-
lance tasks or reaction time may be less environmentally determined
than tests of IQ and seem to be sensitive to impairment by lead, as
mentioned previously. A fruitful approach may be to adapt procedures
proven to be sensitive to the effects of lead in animals, particularly
monkeys, for use with children. Research from the University of
Wisconsin, as well as from our laboratory, has shown consistent ef-
fects on tests of attention and distractibility that could easily be adapted
for children.
Assessment of sensory system function, particularly by psychophysical
means, seems a promising avenue of research and should reflect the
diffuse damage produced by toxicants such as lead. For example, the
decrement in hearing threshold as a function of increased blood lead
(Schwartz and Otto, 1987), although small (and therefore requiring a
large study to detect), undoubtedly represents subtle neuronal dam-
age. It would be extremely interesting to test frequency or amplitude
OCR for page 258
258
DEBORAH C. RICE
difference thresholds in addition to absolute frequency thresholds,
for two reasons. First, there is evidence that difference thresholds
may degrade before absolute frequency thresholds (Stebbins, 1982)
and would, therefore, provide a more sensitive indicator of lead neu-
rotoxicity. Second, the ability to detect changes in frequency and
amplitude is extremely important to the understanding of speech.
Such testing may be especially relevant in view of the reported defi-
cits on auditory processing as a result of lead exposure, reported by
some investigators.
Testing of visual system function may also prove a fruitful avenue
of research. A number of investigations in animals as well as in
workers occupationally exposed to lead report visual deficits, par-
ticularly at low luminance, as a result of lead exposure. Such deficits
probably~could be detected only by psychophysical techniques, because
electrophysiological techniques cannot be used for low-luminance as-
sessment of functions other than purely retinal. Detection of subtle
effects may require testing of a large number of subjects.
Does Head Contribute to Aging?
It is well established from research on animals that lead produces
neuronal degeneration, resulting in decreased numbers of nerve cells
in various brain areas. Developmental lead exposure also results in a
decrease in the amount of dendritic branching from nerve cells, rep-
resenting a decrease in the ability of the nerve to communicate with
its neighbors. It is also established that aging can produce these
same effects. In fact, the brain areas affected most by lead and those
that degenerate most quickly as a result of aging overlap to a great
extent, at least in rodents and monkeys. Although there is presently
no evidence for or against the hypothesis, it is conceivable that the
effect of a lifetime of exposure to low levels of lead results in an
acceleration of the normal process of degeneration of neural struc-
tures. Weiss (1980) discussed the consequences on functional mental
age of a very slight acceleration in loss of functional capacity beginning
at age 25. One-tenth of one percent acceleration would result in a
"brain age" of 95 at 40 years of age (Figure 7~. The actual situation
could in fact be worse for certain individuals, because the deleterious
effect of lead does not begin at age 25 but before birth. Additionally,
the effects of lead on the nervous system of the developing organism
may be more severe and different in kind than accelerated attrition of
neurons.
The effects of lead on blood pressure may also contribute to mani-
OCR for page 259
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
95
85
75
ID
`~ 65
c
._
Cal
co
._
Cal
UJ
55
45
35
25
Al
1 I
, ,
1 ~ ~
b77
it_
. ,
.,
i,0.1%
, ~
-
Effect of n % per year
excess cell loss,
beginning at age 25
1
1
25 35 45 55 65 75
Chronological age (years)
259
FIGURE 7 The "brain age" associated with different degrees of acceleration in the
decline of brain functional capacity, if that decline begins at age 25.
SOURCE: Weiss (1980).
festation of diseases of aging, including heart and kidney disease,
and stroke. The effects of lead on vitamin D metabolism may also
have important lifetime repercussions. As pointed out by Grant (1986),
"this effect is significant on two counts: (i) altered levels of 1,25-
(OH)~-vitamin D not only affects calcium homeostasis (affecting min-
~ . . ~ . O
eral metabolism, calcium as a second messenger and calcium as a
mediator of cyclic nucleotide metabolism), but also likely affects its
role in immunoregulation and mediation of tumerogenesis, and (ii)
the effect of lead on 1,25-(OH)2-vitamin D is a particularly robust one,
with blood levels of 30-50 ,ug/dL resulting in decreases in the hormone
that overlap comparable degrees of decrease seen in severe kidney
injury or certain genetic diseases." Thus lead is implicated in the
compromise of the body's ability to repair tissue, fight disease, regu-
late growth of abnormal cells, and maintain bone, among other effects.
Such functions are often compromised in old age; lead may be con-
tributing to these effects, particularly as a result of 1i-fetime exposure.
OCR for page 260
260
DEBORAH C. RICE
Overview of Cost to Society
Much of the cost of lead exposure is invisible. The consequences
to society of decreasing the IQ of thousands of individuals from 130
to 125 points, or of a few from 160 to 155, are of great significance but
cannot be measured either in monetary terms or in terms of human
suffering. What can be measured monetarily is the cost of inclividu-
als who require special services as a result of undue lead exposure.
Such services may inclucle institutional care, special education, lost
wages, hospitalization, and various forms of treatment. Also included
should be the cost of monitoring children for lead exposure as well
as various abatement programs. An analysis performed a decade
ago (Provenzano, 1980) for the United States estimated the cost at
$0.4 to $1.0 billion (1978 clollars) annually. Since that estimate was
made, the criteria for considering a child at potential risk for leacl
exposure have been made more conservative (CDC, 1985~. It is gen-
erally recognized that blood lead levels above 15 ,ug/dL are undesir-
able for children (cf. EPA, 1984; Grant, 1986~. About 15 percent of
U.S. children have blood lead values above 15 ,ug/dL; the proportion
is higher for poor and black children. This figure translates to 3 to 4
million U.S. children (Mushak and Crocchetti, 1987~. The Committee
on Environmental Hazards (1987) recommends that all children at
risk be tested for undue exposure by erythrocyte protoporphyrin lev-
els at 12 months of age, with later follow-ups for high-risk children.
It also recommends vigorous lead abatement programs. In addition,
the 1978 analysis was performed before the relationships of lead to
blood pressure, vitamin D metabolism, and calcium homeostasis were
known. Thus a modern estimate of the cost would undoubtedly be
substantially higher.
Have Regulatory Agencies Been Slow to Act?
It has been clear for centuries that lead is toxic. It has been clear
for 15 years that lead is irreversibly neurotoxic to children, and for
several years at least that lead at levels observed routinely contrib-
utes to suboptimal behavioral functioning. Various U.S. federal agencies
have been criticized for failing to act to protect the health of the
public (Schoenbrod, 1980; Stein, 1980~. Regulation of lead in the United
States (and other countries) is controlled by a number of different
agencies (Billick, 1981) (Figure 8~. As pointed out by Schoenbrod
(1980), this has provided an avenue for avoidance of action by blam-
ing lead exposure on sources under the control of another agency.
Various agencies have also blamed natural sources, despite the fact
OCR for page 261
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
FEDERAL AGENCY AREAS OF RES~NSIBILIb
Ecodiagrana Showing Movenent Of Lead From The Environment To Man -
Lead Ores (Gabna)
Manutac~ring and
OSHA l,~ Prom
sour
Distribution
1
~ .
Phum~m~s
Health Effects
CPSC
NUT
NSF
HEW
EPA HEALTH EFFECTS RESEARCH
261
Oxop~a
SSU duds
EPA
Airbome Emission
From Autos and
Industry
Gem ssion
Levels
~ ~ Washed by Rain
Soil
Edible Pant Lite
FDA
EPA
Sate L. vels ~ EN
Lead Objects ~
~ ~ l L Paint ~ I
Industrial Wastes
> Rhymers, Lakes.
Oceans
Drinking Water
Plaster (Pea)
CPSC Putty
. Toys
Hazard
Red
FDA Liners /
/
/ Regulation
/ of HUD
_/
| Aquatic Life
POun.v. ME ~ /
~ Inhalation ~ ~ Oral Intake by Man
1
Sate Residue Levels
-
CDC
Gl Absorption - > Feces
Blood ~ Red Blood Cells
(Nondmusible)
\
-
CNS
-
Plasma Ligand ~ Teeth
Bound Diffusive Hair
Bone
(Nondiffusible)
1
Reds ~ ~
Enosphalopathy Peripheral Anemia
Neutopathy
Screening
Body Burden
Treatment
Kidney Mb~ Etre
Tubular Dysfunction Endocrine
Urinary Excretion
Reprodwbve
Cytogenetic
FIGURE 8 Ecodiagram showing movement of lead in the environment and areas of
U.S. federal agency responsibility for control of exposure.
SOURCE: Billick (1981).
OCR for page 262
262
DEBORAH C. RICE
that they contribute considerably less than 1 percent of the human
lead burden (Settle and Patterson, 1980~.
The perceived slowness of regulatory agencies to act is probably
the result of a number of factors. One is the disagreement among
scientists and statisticians working in the field. As discussed above,
the reasons for the controversy are due at least in part to the follow-
ing factors:
Methodological limitations including inadequate markers of lead
exposure, environment-influenced instruments of neuropsychological
function, and choice of populations in which these environmental
factors and lead exposure are highly correlated
· Evaluating the data by simply counting studies as positive or
negative, without looking at direction of effect across studies or power
of individual studies to find an effect, and failure to perform meta-
analyses
Failure to utilize the animal literature in interpreting data from
human studies
· Failure to recognize that a "small" effect (i.e., 2 to 3 percent of
variance) does not translate to "insignificant"
In addition, there may be a reluctance on the part of regulatory
agencies to regulate on the basis of psychological test data. For ex-
ample, the EPA has focused on the effects of lead on heme synthesis
and the hematopoietic system (EPA, 1984) and, more recently, on
vitamin D metabolism (Grant, 1986~. This may represent a real reluctance
to regulate on the basis of behavioral data; conversely, regulators
may be sensitive to the potential legal ramifications of the controversy
over low-level effects on psychological functioning. It is hoped that
recent studies demonstrating effects on behavior and intellectual
functioning in middle-class children at blood lead levels typical in
our society, as well as the analyses based on the NHANES data, will
persuade regulatory agencies in their decision-making processes.
CLOSING PANDORA'S BOX
The level of lead in the environment in bioavailable form, distrib-
uted over the entire earth, has been increasing for thousands of years
as a result of human activity. The industrial revolution accelerated
the release of lead into the environment. The use of lead in paint still
produces undue lead exposure in children, as a result of old paint in
old houses and the present use of lead in paint for application to
OCR for page 263
HEALTH EFFECTS OF ENVIRONMENTAL LEAD EXPOSURE
263
metals. The decision in the 1920s to add lead to gasoline has resulted
in virtually universal exposure of the entire populations of industri-
alized countries. Humans now carry a lead burden 500 times that
before lead mining began, and present intake is 100 times greater.
The United States has legislated the phaseout of lead from gaso-
line, and other countries are doing the same or contemplating such a
move. Lead abatement and monitoring programs are in place in the
inner cities, and children are being "treated" (by chelation) if exposure
to lead reaches a specified level. The average level of lead in the
blood of children as a result of these actions has decreased since the
mid-1970s and will undoubtedly decrease even further. Can we therefore
congratulate ourselves on our success in alleviating the problems produced
by lead exposure and feel confident that lead toxicity will soon no
longer be an issue to contend with? The answer is, unfortunately,
no.
The adverse effects of in utero lead exposure are being character-
ized. The women presently in their childbearing years, and those
that will be for the next 20 years, have been exposed during childhood
to the highest lead levels since certain ancient civilizations. These
individuals presumably carry a high level of lead in bone, which is
available for mobilization into the fetus. In addition, there are millions
of individuals who have had undue lead exposure as young children.
Even if their exposure to lead decreases substantially, permanent damage
has already been done. These individuals will be part of our society
for another 60 to 70 years.
The effects of lead on various biochemical functions, particularly
calcium homeostasis, may stress a wide variety of functions over the
course of the life span, resulting in premature breakdown of these
functions and accelerated aging. The ongoing insult of lead to the
brain may also result in an accelerated decrease in mental function-
ing. These deleterious effects would presumably manifest themselves
for a considerable period of time in our populations even if lead
exposure ceased tomorrow.
It is clear, then, that environmental lead indeed represents a chemical
time bomb in two senses: First, exposure to lead over years or a
lifetime may result in health effects late in life, as well as very early
in life. (We cannot know this yet, because individuals exposed in the
1940s and 1950s will not reach old age until after the turn of the
century.) Second, decisions made by industrialists and governments
in the 1920s and before will have unavoidable effects on individuals not
yet born. It will be at least one more generation before this particular
Pandora's box can be closed.
OCR for page 264
· 264
DEBORAH C. RICE
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Representative terms from entire chapter:
lead exposure
