Ted Tjossem of NICHHD called me last week to ask for some data to use in briefing you on the prevalence of lead exposure and
resultant brain impairment. I had intended to bring this matter to your attention at some time after you had settled in more
firmly, but he told me you have a special interest in preventing mental retardation. I hope to persuade you that lead exposure
is one of the commonest causes of preventable mental retardation and that it is one cause whose complete and permanent remedy
is presently within our grasp.
This interest in lead goes back to when I was chief resident at CHOP. That year we admitted more cases of plumbism than ever
before, simply because I pressed the residents to do what Bob Kaye and Al Bongiovanni had taught me - think of lead poisoning
and then draw a blood for lead in the summertime whenever you see an anemic child, a constipated or irritable child or one
with abdominal pain. I became convinced then that there was more lead toxicity than recognized.
I want to make the following points:
1. The threshold for lead effects in children has been lowered from 60 ug/dl to 30 ug/dl in the face of a growing body of
epidemiological evidence. It will probably be revised further downward.
2. Animal studies have supported the epidemiological data.
3. Lead encephalopathy has decreased dramatically, but the incidence of excess exposure to toxic doses of lead is higher than
anyone had expected.
4. Lead is a teratogen, and in utero exposure may be a Health concern.
5. Lead may also be involved in the disturbed mentation that can accompany aging.
6. The monetary costs for low level lead exposure in children are probably well in excess of $1 billion per year.
7. Effective prevention is no mysterious problem. It is simply a question of proper determination and good planning.
1. The threshold for lead effects has been lowered. This is still an area of controversy. A number of studies have shown health
effects at lower doses, some have not. In 1974, I showed, with Ed Sewell's help, that dentine lead levels in the lead
belt of Philadelphia were five times as high as those in the greater northeast and that 20% of the inner city children had
dentine lead levels in the range associated with frank toxicity. In 1979, my group, using this marker showed that asymptomatic
children with elevated dentine lead levels had lower IQ scores, lower scores in auditory and language processing, and impaired
attention. Teachers, blind to their lead level found high lead subjects twice as often to be distractible, disorganized and
less able to follow directions. EEG records or a subsample of high lead children had less midline alpha and more midline delta.
The mean blood lead in my high tooth lead group was 35 ug/dl. We have followed these children, now fifth and sixth graders,
and their school performance remains impaired. Other studies in England and in Germany have since confirmed these findings.
2. Animal-models confirm the epidemiological studies. Lead effects on brain adenyl cyclase on synaptogenesis and brain cytochromes
have been shown at very low doses. Behavioral changes have been demonstrated in the rodent and the non-human primate.
3. Lead encephalopathy has decreased, but undue exposure is appallingly high. The recent National Health and Nutrition Examination
Survey (NHANES II) conducted by the National Center for Heath Statistics and FDA was in part a carefully designed study of
blood lead levels in a representative sample of Americans. The methodology is very sound. None of us who worked in the field
expected that the prevalence of exposure would be as severe as the data showed. For example:
[TABLE = (Percentage of Children 6 months - 5 years with Blood Leads 30 ug/dl)]
This means that over 600,000 children in the U.S. have blood leads in the dangerous range, that 180,000 black children are
at serious risk. It shows that lead is not a problem for blacks alone, but that race and poverty increase the risk dramatically.
4. Lead is a teratogen, and in utero exposure is a concern. A number of studies have shown lead-induced neural tube anomalies.
Lead crosses the placenta, and fetuses are more sensitive than more mature organisms.
5. Lead may be involved in the psychopathology of aging. The largest partition of lead is in the skeleton, where it is assumed
to be inactive. With advancing age, the skeleton demineralizes. Where does the lead go? Is it possible that some of the disordered
mentation associated with aging is lead induced and therefore preventable?
6. The monetary costs attributed to lead exposure are huge, probably well over $1 billion per year. Cowan and Leviton using
my data, estimated the population attributable risk for poor classroom behavior due to lead as 43%. That is, in Somerville
and Chelsea, Massachusetts 43% of the low overall functioning in the first grade could be attributed to elevated lead exposure.
Suppose they were incorrect by a factor of 3, and 14 of the poor behavior was lead attributable. This is still a striking
Provenzano, an environmental economist, estimated the costs in 1978 dollars for remedial education and medical care as ranging
between $400 million and $1 billion. He felt this to be conservative. The range requires revision in light of inflation and
the altered prevalence figures documented in NHANES II.
7. Effective prevention is no great problem. Lead is easy to measure in the environment and in humans. I do not believe we
need debate any longer that it is a powerful and pervasive neurotoxin. It should be removed from the human environment to
the technological extent possible. The important sources are:
a. Houses (old paint is still around)
b. Air and dust (gasoline and factory emissions)
c. Food (cans and processing)
d. Water (in some areas)
If anyone had told me when I entered medical school that smallpox would be nonexistent in 1980, I would have thought them
silly. It is not farfetched to visualize eliminating lead intoxication and its attendant effects on children's brains
from American society forever. You possess the kind of vision that could accomplish this. There are a number of fine people
in HHS who have been working hard on this issue and are very informed. If I can be of use, please do not hesitate to let me
know. I would like to come to Washington to talk with you further about this.
Herbert L. Needleman, M.D.
Associate Professor of Child Psychiatry and Pediatrics