Call Transcript
1. Introduction: Eleni Sotos, MA, National Coordinator, Collaborative on Health and the Environment
Good morning, everyone. Welcome to the June National CHE Partnership call, titled, “Getting The Lead Out: The Latest On Lead Exposure and Health Outcomes.” My name is Eleni Sotos. I’m the National Coordinator of the Collaborative on Health and the Environment. The moderator for this call will be Michael Lerner, President of Commonweal, and Cofounder of CHE.
I’m very pleased to introduce today’s guest speakers. First we will have a science update from Dr. Pete Myers -- CEO of Environmental Health Sciences, publisher of Environmental Health News and co-author of Our Stolen Future.
Next, we are honored to welcome Dr. Herbert Needleman, a pediatrician and child psychiatrist at the University of Pittsburgh Medical Center. His pioneering research on the effects of lead on child development over the past 30 years has led to far-reaching policy implementation from the CEC issuing guidelines for the diagnosis and management of lead poisoning in children, to the Consumer Products Safety Commission banning lead from interior paints.
Dr. Needleman is also the founder of the Alliance to End Childhood Lead Poisoning, an education and advocacy organization, which aims to reduce the hazards of lead-based paints in the homes of inner-city residents.
Next, we will hear from Dr. Kim Dietrich, the Associate Director of the Children’s Center for Environmental Health at the Cincinnati Children’s Hospital Medical Center, and Director of the Division of Epidemiology and Biostatistics. Dr. Dietrich’s research has focused on the developmental effects of prenatal and early postnatal exposure to lead in infants, toddlers and school-aged children and adolescents. He is also examining the effects of prenatal exposure to prevalent developmental toxicants -- including lead, pesticides, mercury, PCBs, tobacco smoke and alcohol a birth cohort of 400 infants.
Finally, we are pleased to have CHE Partner Neil Gendel, Project Director of the Healthy Children Organizing Project, to offer his comments and questions as responder to the presentations.
2. Moderator: Michael Lerner, PhD, President, Commonweal
Our first presenter is Pete Myers, with a science update.
3. Science Update: Pete Myers, PhD, CEO Environmental Health Sciences
This has been an extraordinary month in scientific publications on environment and health. It’s been a non-stop parade of new findings being announced, that range from studies on phthalates as related to the use of equipment in neonatal Intensive Care Units to very important studies of level effects of bisphenol A on reproductive-tract development of prostate in males and mammary gland tissue in females. Including the latter folks significant results of mammary gland reorganization at 25 parts per trillion.
Another study looking at multigenerational transfer of fertility impairment via DNA methylation epigenetic mode of action down to four generations.
Two human studies have emerged in the last few weeks, which I think are of special importance. They are particularly important because these were studies conducted by epidemiologists who designed their work based on follow-up of experimental results from animals. One of those studies -- by Dr. Shanna Swan and her group -- looked at phthalate exposure linked to genital malformation in baby boys, and found heart defects at phthalate levels to which 25 percent of American women are exposed, according to Centers for Disease Control data. The odds ratios were extraordinarily high for epidemiological studies.
A second result received a lot less attention than this one -- but I think is also quite important. Just on Friday, a Japanese team of researchers released studies published in human reproduction that link bisphenol A lead exposure. Bisphenol A is a compound that leaches out of polycarbonate plastic to which 95 percent of Americans are exposed. Their results link bisphenol A exposure to recurrent miscarriage in women.
This was a prospective case control study with a relatively small study group. But they were able to show that women with higher levels of bisphenol A were more likely to have subsequent miscarriage. They also found that the aborted fetuses from the women who miscarried in the pregnancy that they were tracking carried signs of cellular damage consistent with the animal results. That is, they were aneuploid -- which is an error in cell division, and is the largest known cause of spontaneous miscarriage in people.
4. Featured Presentations
Michael Lerner: Pete, thank you very, very much for a very informative science update. Our first speaker, Dr. Herb Needleman, is a great pioneer in the field. Dr. Needleman was also a keynote speaker at the wonderful initial conference of CHE-Penn in Pittsburgh. Dr. Needleman, we’re honored to have you here.
First Speaker: Herbert Needleman, MD, Professor of Psychiatry and Pediatrics at the University of Pittsburgh School of Medicine and Founder of the Alliance to End Childhood Poisoning
It’s a pleasure to be here. Let me begin by describing five phases of our understanding of childhood lead poisoning. Initially, it was not believed that children were affected by lead. That was dissipated in 1892 in Australia, when the first cases of childhood lead poisoning were reported. After that, the prevailing belief was that there were only two outcomes from lead poisoning, either death or a complete cure. If it didn’t kill you, it didn’t touch you.
Then in 1943, Randolph Byers at the Boston Children’s Hospital followed up children who had recovered and were supposedly cured to find that 19 out of 20 had severe deficits in learning or in behavior. Then the long-term effects of lead were accepted. But they were only thought to occur in children who had frank signs of encephalopathy. In the 70s and in the 80s, many studies from around the world showed that children who had no visible symptoms but had elevated body burdens had impaired cognition, attention and language function. So the long-term consequences of lead were then accepted in silent exposures.
I think we’re in a 5th stage, which is different. Most of the studies in the past focused on cognition -- IQ -- because it was easy to measure. But Byers began his first studies because he was referred two children who had attacked their teacher. Not children who were failing in school. So the behavioral consequences and social adjustment and violence have now come under study. I have shown that children who had high lead in their bones had impaired function on the child behavior checklist. Then more recently in a case-control study of 195 delinquents and 145 controls, we showed that the bone lead levels in the delinquents was nine times what it was in the controls.
I think there are other things that are unfolding in lead. When I started in this field, the threshold for effect was defined as 60 mcg per deciliter. It was very easy, if you were a pediatric resident as I was. If a child had a blood lead of 60, you treated him. If he had a blood lead of 59, you followed him.
Over time, because of the studies of children’s effects at low dose, the federal definition of lead poisoning has shifted down from 60 to 35 to 25 to 20 to 10. There are good studies now that show effects below 10. The surprising thing is that the slope of the IQ deficit in relation to blood lead is steeper below seven than it is above seven.
That sounds paradoxical. It sounds like it violates the dose response curve. But it doesn’t. What it projects to me is that there are certain targets for lead that are exquisitely sensitive and are easily saturated. So they are filled up. Then other toxic effects have to come into action at higher dose.
The pooled study that Kim and I were involved in showed this effect. When we examined our data from Boston, we found the same thing. In the more-recent publications, Steve Rothenberg did a very eloquent statistical analysis, which shows that the slope below five is very steep, and that an equal amount of damage is done in going from one to five, as it is in going from five to 10. The importance of this, I think, has yet to be understood.
I just want to say that there are many reasons the directed prevention of lead toxicity has fallen way behind what we know. It was assumed to be a disease of poor people and of minorities. So it didn’t get the attention it should. The mothers were accused of poor care giving and thus being responsible for lead poisoning. Academic pediatrics has ignored, in general, lead effects at low-dose. It’s not as exciting as molecular biology. And the lead industry, of course, has weighed in on this with a lot of money and a lot of influence.
The other thing is that when you talk about lead toxicity, people say, “Why are you worried about it? Haven’t we passed a law forbidding lead in paint? And didn’t we take it out of gasoline? The problem is over.” Well, of course, that’s not true. The more recent studies document that there are still large numbers of children who are experiencing toxic doses of lead.
The same time as people say that, they also say, “Well, we can’t afford to deal with it.” The economic benefits of taking lead out of gasoline have been shown to be enormous. If we were able to reduce the ambient exposures to lead even more, there’s no doubt in my mind that the calculus would be positive, and in favor of removing lead.
Michael Lerner: Thank you very much, Dr. Needleman. Dr. Dietrich?
Second Speaker: Kim Dietrich, PhD, Associate Director of the Cincinnati Children's Environmental Health Center at Cincinnati Children's Hospital Medical Center
Thank you. I want to just say that it’s a privilege to be on a panel or call with Dr. Needleman -- who’s really been the leader in this area of modern lead research.
Dr. Needleman has given an eloquent history of the problem of lead, from around the turn of the last century.
One would think -- particularly after hearing from Dr. Needleman -- the long history of the lead problem -- and the awareness of the lead problem, after all these years of research -- that there might be little to add to this lead story. But what we’re finding is that this ubiquitous toxicant continues to amaze -- it amazes me, anyway -- and also concern those of us who continue to investigate its impact on the health and development of the fetus and child. As these studies go forward, we’re finding that early exposure to lead has consequences that extend into adolescence, and now into adulthood.
We have a number of research studies underway here at the Cincinnati Children’s Center for Environmental Health that are related to the impact of lead on human development. The particular focus we have now, however, having already published the effects of lead on reproduction, fetal development and infant / preschool development. Our focus now is on the effects of prenatal and early postnatal lead exposure on the neuropsychological functioning and social adjustment of young adults.
To examine this question, we’ve been engaged in a continuous follow-up of a birth cohort that we recruited prenatally, between 1979 and 1984 in Cincinnati. Sometimes this study is referred to as the “Cincinnati Lead Study.” This is a birth cohort that was recruited from an area within Cincinnati that has had historically high incidence of cases of lead poisoning and even fatalities in the 40s and 50s and early 60s.
I would like to briefly describe two studies that we have underway, and some results that we have recently recorded at some national scientific meetings. We presently have two studies underway now that the members of this Cincinnati Lead Study cohort are involved in. I would just remind everyone that this is a long-term study. This cohort is now in their early- to mid-20s. So when we talk about the effects we see, we’re talking about the effects of lead that have persisted into adulthood.
The first study is in examination of the relationship between early exposure to lead and adult criminality. The other is a study of lead’s effects on the morphology and functional neuroanatomy of the brain, using various magnetic resonant imaging or MRI techniques.
As far as the study that we’re doing on this cohort, with respect to early exposure to lead and adult criminality, we recently reported at the national meeting of the American Society of Criminology Conference in November. My colleagues include a criminologist by the name of Dr. John Wright and a clinical neuropsychologist by the name of Dr. Douglas Ris. Both of these people are here with me at the University of Cincinnati.
In this study, we were interested in the relationship between early exposure to lead and various measures of adult criminal behavior. Such as, for example, the frequency of police contacts, arrests and incarcerations in our Cincinnati Lead Study subjects.
What we found and reported at the Society of Criminology meeting is that after adjusting for a number of covariants, including a vast array of social and medical and economic factors, and even their parents’ criminal history, and even their own previous record of delinquent acts, when they were around 15-16 years of age, we found that their blood lead levels during the first six to seven years of life predicted adult criminal behavior -- as documented in the official records of the counties in which these subjects resided. It was a very strong and robust relationship.
Some would argue that we actually over-controlled this analysis. We controlled for parents’ criminal record history. We controlled the subjects’ own delinquency history and also, their IQ -- all of which could be outcomes of lead. Nevertheless, even in the face of these so-called co variants or confounders, we found lead to be a robust predictor of these measures of official documentation of criminal behavior in adulthood.
Another intriguing finding from this study, which gets at something that Dr. Needleman has brought up in meeting after meeting is that lead is really a transgenerational toxicant. One indication of that was this intriguing finding in the same data. The blood lead levels of the subjects’ mothers during their pregnancy with our subjects predicted criminal history - Thus, suggesting that lead may be one of those variables responsible for the intergenerational transmission of criminal behavior.
This is the idea that if your parents engage in crime, you’re more likely to engage in crime. It’s nothing new. This has largely been based on theories that are mainly sociological and psychological in nature. To my knowledge, no one has ever suggested that an environmental toxicant can also be playing a role in the intergenerational transmission of anti-social and criminal behavior.
The paper that this is based on has not appeared in print. If you’re interested in the abstract that was published in the journal, The Criminologist, we hope to have a more-complete report published in the near future.
As I mentioned before, we’re also studying the impact of early lead exposure on the morphology and functional neuroanatomy of these subjects using MRI. One of our first reports was presented last month at the International Society for Magnetic Resonance Imaging that dealt with the influence of childhood lead exposure on language functioning in these same young adults. We used a technique called “functional MRI.” With MRI, we can measure the blood oxygen level dependent activation of various areas of the brain, while the subject is engaging in a cognitive or motor task. This work was lead by Dr. Cecil, at Cincinnati Children’s Hospital, in collaboration with others and myself.
We utilized the Verb Generation Test. In this test, the subjects generate verbs that are associated with a noun. For example, if they hear the word, “ball,” they have to think of verbs that are associated with it -- like, “Throw, kick,” and “hit,” and hit a button as they’re thinking about that. What we found from the results of this study was that the elevated childhood lead exposure influenced the neurosubstrates of semantic language function. I could show you exposure-dependent, atypical, abnormal organization of language functioning in these adults with a history of childhood lead poisoning.
But what’s interesting about this is that to my knowledge, this is the first direct evidence of neuroanatomical reorganization of the brain as a result of early lead exposure. And of course deficits in verbal and language behaviors and verbal reasoning have been associated by criminologists and people who study juvenile delinquents with deficits in verbal behavior.
There are some other issues that may be going on here, as well -- such as premature aging of the brain, and the fact that the language dominance appears to be evening out or decentralizing in the brains of these lead-poisoned kids, long before they should be -- which would normally be in the 30s.
Michael Lerner: Thank you very much Dr. Dietrich. Dr. Needleman -- at the Pittsburgh CHE Conference, you made 2 additional points that I just want to ask you if you would comment briefly on. The first was on the future of lead research, which relates to the comment Dr. Dietrich made on premature aging of the brain. It had to do, I think, with an animal study of plaque-like formations. The second point, just very briefly, was that you felt lead might be an example -- not unique -- of what we might discover if we looked in greater depth at other contaminants. I just wondered if you would comment briefly on this.
Herb Needleman: Certainly. Well, Nasser Zawia at the University of Rhode Island gave small amounts of lead to one-day old rats. They measured their amyloid precursor protein levels, which went up but then came down to normal. Then at age 21 months -- which is old age for rats, the APP came back up. So he thinks this is an example of reprogramming of the genes for amyloid, and may be a part of the Alzheimer’s disease pathogenesis. It’s something that we’re going to pursue, and I think Kim might want to do that, too.
The thing about lead is, it’s easy to measure. You know where it is and it sticks around. So the marker is always there. As a consequence, it’s a best-study toxicant. But I think that the same kinds of possibilities extend to pesticides, certainly -- to phthalates, to bisphenol A. If we examine them with careful measures and large-enough sample sizes, I have no doubt we’re going to be finding neurotoxic effects.
Michael Lerner: Thank you very much. Neil, would you please take a few minutes to frame some broader issues and ask some questions for the start of the comment period?
Responder: Neil Gendel, Project Director, Healthy Children Organizing Project, Consumer Action
I’m very glad you asked that question of Dr. Needleman, because I really think that our experience with childhood lead-positioning prevention efforts may raise questions for me in terms of where we’re going with all these other toxics.
The Healthy Children Organizing Project began with the Childhood Lead Poisoning Prevention Project in 1990. We were facing a city literally painted with lead and plenty of other sources of lead -- both ethnic sources and leaded gas.
We didn’t have any guidelines to follow. Very few people knew anything about lead. Herb Needleman’s wonderful work and other researchers’ work was just beginning to seep into our knowledge. We decided we needed to do a citywide effort, because there were a large number of low-income and working poor communities-of-color in San Francisco. We began with some guiding principles, and that was with everybody serving families and children were responsible for helping to have healthy, non-leaded kids. That included all city agencies that provided family and children services, property owners, community-based organizations and others. We also believed that while education and awareness are good, we need healthy lead-safe homes and public facilities, to have any chance of solving the problem in the long run.
We used some legislation in 1992, with some collaborations in partnerships driving it, to put together a blueprint for city agencies to make their facilities lead-safe and educate persons they serve. We also set up a process to figure out how to make private housing lead-safe for the kids. We put together several mechanisms to encourage the implementation of this legislation, which we are still working on 13 years later.
That means we formed a partnership with the Department of Public Health to do a number of things besides just this case management. We created a city agency task force to clean up their facilities. We created a citizens advisory committee to monitor the work of the city agencies, and we created a citizens advisory committee to begin to recommend legislation to clean up housing in the city. That included property owners, contractors, tenants, unions and many other people who were stakeholders in the condition of property in the city. In addition to that, we found funds in a variety of ways to clean up childcare centers, and to do outreach and education -- and put together brochures, one of which was distributed to over a million people in California, because a lot of other people liked it. We had no particular expertise at that time, because there just wasn’t that kind of information out. There is much more, today, as you can see.
The results are that we can say that the housing authority’s facilities look a bit better, these days through the schools. The recreation and park facilities, where thousands of children under the age of five go every day are much better. We have “safe work” practices for interior and exterior homes in childcare facilities here in San Francisco -- one of the few places in the country. This is what the EPA was supposed to have been doing. You may have heard some flak about it, because they’re about nine years late and haven’t even started.
At the Healthy Children Organizing Project, we are very aware of children -- in particular, in their own homes -- living in what many of us refer to as the “toxic soup,” of the problem. They need to do something about it. So the question is, “Where are we going today?” How can we reach low-income parents -- many of whom don’t speak English very well, and don’t get their information from the Department of Public Health or other traditional sources? With the research information being generated by our speakers today, we’re doing wonderful work. That will change a parent’s behavior. That last phrase is very important. You can’t just throw pieces of paper at them. We know that.
How do we get public and private property owners to make homes healthy for tenants and themselves, and public facilities healthy for children and adults? Those are two very important questions, which we continue to struggle with.
5. Questions/Comments/Discussion
Michael Lerner: Neil, thank you very much. We welcome comments and questions, please.
Philip R. Lee, MD, Professor Emeritus of Social Medicine, UCSF and the Institute for Health Policy Studies, Stanford University, Program in Human Biology:
Herb, thank you for joining us today, we appreciate everything you’ve been doing. I would like to ask a question about your comment about other toxic potentials. I’ve been very interested in manganese. Very similar problems seem to be arising that studies are not nearly as well-done, or over as long a period of time. But there is some suggestion about more lead in water. I wondered if you would comment either on the preventive end of this and how we can approach the multiple toxin problem. Secondly, regarding preventive measures, we know about housing and we know about lead in paint. Aren’t there still issues about lead in water and public water supplies?
Herb Needleman: I think that’s coming back into awareness. Yes. I think it has to be examined very carefully.
Philip R. Lee: With the manganese, there’s a lot of evidence that if the woman is anemic or has low calcium, the problems are magnified significantly in the kids, in terms of manganese. The behavior is very similar. They end up in jail. They have violent behavior. It’s various other related problems.
Herb Needleman: I think manganese follows the same patterns as lead. It was first discovered in workers. Manganese workers have a high rate of psychosis and brain damage. The question is, does it extend at lower doses to the communities? I think it just needs a very good epidemiology. I don’t think there is very good epidemiology on the issue, yet.
Philip R. Lee: There’s some EPA data. A professor at UC Irvine, actually, is looking at EPA data on manganese in the air, in areas where there are manganese smelters. Those areas have the highest levels of violence anywhere in the country, apparently. It’s truly amazing.
Ernest J. Sternglass, PhD, Professor Emeritus of Radiology, University of Pittsburgh School of Medicine:
This question of the multiple contaminants is very interesting, because Pellegrini at San Jose State University in 1987 published a paper showing that radioactive fallout from bomb-testing had had similar effects on criminal violence. Also, which is interesting, which we’ve discovered in recent years, is the non-linear response that it rises much more quickly at very low doses, and then levels off at high doses. The large prevalence of fallout and releases, which are permitted now from over 100 nuclear reactors, clearly must be a measure of great concern, as we have been showing.
Sandy Ross, Health & Habitat: How do we stop the intergenerational situation, when we look at it from an epigenetic standpoint?
Kim Dietrich: Well, to some extent, all of these problems boil down to primary prevention. One of the reasons why I think we’re seeing what we’ve observed in our studies is that the mothers of these children now adults, lived in the same house as their children. That is, they were living in older housing, generally in poor condition, and were becoming exposed to higher levels of lead, as well. As a matter of fact, some of the mothers in our study show up on our old health department lead-poisoning rolls. To the extent of the exposure in the first place, we are breaking that connection.
Herb Needleman: I used to make house calls on families on my intervention study. You cannot imagine the squalor in which some people live, in American cities. If you go through those neighborhoods, which I’ve done, you see it’s the same place where there are bad houses; there are a lot of unemployed people.
The natural response to that would be to take unemployed people, and train them in safety. For the same dollar, you get three effects. You make a house livable, you put somebody back on the tax rolls, and you wipe out lead poisoning forever. Each time we de-lead a house, it’s safe for the entire life of that house, which may be 30 or 40 years. And five or 10 families might live in it.
This makes such good sense that Dave Jacobs at Housing and Urban Development Department was trying to do that. But you saw what happened to Dave Jacobs.
Kim Dietrich: We need to do that at the community level. It’s not enough to do what we’re doing now -- it’s piecemeal. We’ll de-lead a house or rehab a house on a block -- one house on a block, where it’s surrounded by other homes that are thoroughly contaminated. That house that you de-lead becomes re-contaminated over a very short period of time. It can’t be done piecemeal. It has to be done by blocks -- by neighborhoods. Not these small grants for one home at a time within an island of lead.
Herb Needleman: That’s an amazing employment opportunity.
Kim Dietrich: Absolutely. We had these mechanisms at one time. The block grants and things like that, which were wasted. There are mechanisms to do this, if there is a political will and willingness to do this.
Mark Mitchell, MD, MPH, President, Connecticut Coalition for Environmental Justice:
I had a different type of question for Dr. Needleman, he being a pioneer in the toxics area. I think he was subject to a lot of attacks and trying to be discredited. I wanted to know how you have come to be recognized, as you are, now.
Herb Needleman: Yes. I was accused of scientific misconduct, from people in the lead industry. We went through a big, involved process here at Pitt, and they found out that there was no scientific misconduct. I wrote a piece on that in Pediatrics, I think in 1987 or 1991. It was called, “Salem Comes to the NIH.” You can look it up under my name.
Philip R. Lee, MD: Herb, it’s important to note that it wasn’t just the lead industry. In fact, NIH participated in that, did they not?
Herb Needleman: NIH and the University of Pittsburgh.
Question from the San Antonio and also the State of Texas Childhood Lead Poisoning Prevention Program: In San Antonio, we are running into a problem. I just finished a large assessment with K-12 science teachers that are in other general disciplines as well, regarding environmental exposures, and how it’s affecting learning disabilities and behavioral problems in their classrooms.
We made a large discovery that many of the children who have been placed on ADHD medication and/or have been put in special education classes are truly just lead poisoned. As soon as we remove the exposure and the blood level drops, the children perform normally in normal classrooms. And of course, this is becoming a big issue with the Texas Education Agency and others -- because it’s a huge cost. Are there any studies out there or any comments regarding that?
Herb Needleman: There are many studies in the literature that show that lead is involved in impaired attention, irritability and fidgetiness.
Tom Lent, Healthy Building Network: I just wanted to remind everyone that lead is still a problem. We still have a very active lead industry in the buildings that we see. We see it in PVC as a stabilizer. It’s in the wiring that goes into every new house, as well as being widely used in solder -- amongst other uses. There are ongoing new sources of lead going into the environment, steadily. This is just a legacy problem we’ve got with paint.
Cheri Joseph: I have a question about the third-world imports of kitchenware and drinking cups and glasses and cute plates that are painted for Christmas. We have a proposition here in California that people have to be warned if they may not be safe for food consumption -- if there’s anything being done on that. I’m concerned about the glazes having lead in them or other toxicants, and what’s happening with that situation.
Herb Needleman: Periodically, the Consumer Product Safety Commission issues a bulletin warning about one of those sources. Dishware from Mexico and from Europe should not be used for food, without doubt. Chinese jewelry that they have in vending machines has a high lead content. There are many sources.
Neil Gendel: The Attorney General brought a lawsuit against the major manufacturers of tableware that were sold in many of the department stores here in California, probably about eight years ago. They are required, if their tableware tests above a certain rate, to mark the tableware as not being usable for human consumption.
What’s been said about coming across the borders from Latin America and the Far East is absolutely correct. There are ways to test that tableware. But even if you have tableware that tests okay for a while, as it ages, there’s a lot more reason to believe that tableware that hasn’t been fired properly will deteriorate, and you can be exposed to lead.
Deborah Moore, PhD, Executive Director, Second Look: I’m wondering if Dr. Needleman, in particular, knows anything about the research that’s come out about chloramines and fluorosilicic acid. Which are a combination of -- I guess -- of chlorine and a water-supply disinfectant, and fluorosilicic acid, that’s put in as a purifying agents.
Herb Needleman: I think Roger Masters at Dartmouth is concerned about that.
Deborah Moore: This is brand new research that’s been done. I think it’s pre-publication. But this has been done by Richard Maas, from the Environmental Quality Institute at the University of North Carolina.
Herb Needleman: Did you say it increases the uptake of lead? Is that it?
Deborah Moore: Well, I don’t know if he gets into that end of it. I haven’t read the actual research. He’s done a news report on it, and I’ve heard indirectly from him. But the chemical interaction could be responsible for the elevated blood levels.
Jim W. White, Toxicologist, Office of Environmental Health Assessments, Washington State Department of Health:
I was wondering if Drs. Needleman and Dietrich might comment on the strength of the data that’s suggested it’s not just young kids, but also school-aged kids and teens that are vulnerable to the effects of low-level lead exposure?
Kim Dietrich: One of the papers that we published in the Environmental Health Perspectives -- I think it was last month -- looked at the question of sort of the critical periods of exposure for children, in terms of having an impact on their intellectual functioning and academic achievements. What we looked at was whether or not it’s just exposure or elevated blood lead levels during -- let’s say -- two to three years of age that are important or critical to later problems. Are older children at-risk, as well?
You can read in the papers, and it’s posted on the websites, but what we found was that there was in fact a very strong effect of concurrent blood lead levels. That is, blood lead levels when children were seven or seven and a half years of age, on their IQ. Even after adjusting for their previous blood lead levels. The effects of later blood lead levels -- even at lower levels below the CDC guideline -- may be more important than previously believed.
So this idea that once a child is beyond three or four years of age, you no longer have to be concerned or screened because it’s no longer important, may be one that we need to reassess or revisit.
Herb Needleman: I think Kim is absolutely right. There’s nothing about becoming 13 and bar-mitzvah’d that immunizes you against lead poisoning.
Lorraine Eckstein, PhD, Research Anthropologist, Alaska Community Action on Toxics (ACAT):
Can we treat medically people with the amount of lead in their bodies?
Herb Needleman: There are a number of chelating agents that lower high blood lead levels. But as Kim is responsible for the psychological evaluation of its efficacy, it doesn’t do anything to protect IQ at lower doses.
Mark Mitchell: CDC has kept the blood level of impairment to be safe at 10, even though there’s evidence of effects below 10. Do you think that they should declare that a safe blood lead level is zero?
Herb Needleman: I think it’s an empirical question. There’s very good evidence that it affects occur below 10. I think that the policy should adjust to the science. However, when the CDC began to look at this a year or so ago, people were kicked off the committee by the Bush administration, and Dick Jackson was forced out of his position as director for the National Center for Environmental Health. These are the realities of trying to do good, at this time and in our history.
Philip Lee: I have another question that has to do with the research agenda. What should be a research agenda? There are a number of foundations with interest in this area. It’s unlikely we’re going to get a lot of action either at NIH or at CDC in the short-term, but we need to really look at where we ought to be going. Would you make a couple of suggestions about that, Herb and/or Kim?
Herb Needleman: I think what Kim is doing is following that up on that with a very-carefully assessed cohort. It’s the direction we should be going in. I think that the effects of early lead-exposure on diseases of late life are really important areas for scrutiny.
Michael Lerner: I think we are at the point where Eleni should give us some last words. Again, thanks to our speakers, Eleni, do you have any last words for us?
Eleni Sotos: I just want to thank Drs. Dietrich, Needleman, and Neil Gendel for coming on, as well as Pete’s update. I just want to note that we will be announcing the next call next month in the next week or so. So keep an eye out for an e-mail announcing that next call. If anyone has any additional questions or comments about this call, feel free to forward them to me.