Learning and Developmental Disabilities
1. Introduction and Overview of the Learning and Developmental Disabilities Initiative (LDDI): Elise Miller, M.Ed., Executive Director, Institute for Children's Environmental Health and National Coordinator for the Learning and Developmental Disabilities Initiative
LDDI coalesced at the first meeting of CHE, almost two years ago, when we gathered to discuss how researchers, health care providers, health affected groups and advocacy organizations might work together more effectively given the growing concern about environmental contributors to chronic diseases and disabilities. A number of people highlighted their concerns about neurotoxicants, such as lead, mercury, PCBs, poly-brominated flame-retardants (PBDEs), solvents, etc., and about the apparent rise in numbers of children with various learning and developmental disabilities--noting about 1 in 6 children are now struggling with some form of these disabilities. Given this specific interest in toxics and neurological development, we determined that the LDD sector, with its hundreds of thousands of members, in collaboration with scientists and key environmental health and justice organizations, could be a very effective voice for protecting children from toxic hazards related to brain development.
At our first meeting in Washington D.C., we developed three major goals: 1) to educate state and national LDD groups about possible environmental links to these problems and the need for preventative efforts, 2) to raise awareness amongst the groups' broader constituencies through various workshops and presentations and development and dissemination of materials, and 3) to cultivate opportunities for interested organizations to educate legislators on specific bills that would eliminate neurotoxicants.
We now have 100 individuals and organizations involved in LDDI, including: The Learning Disabilities Association, The American Association on Mental Retardation, The Arc of the United States, Safe Minds, The Autism Society, The National Literacy Foundation, Communities Against Violence Network, and more.
Some of the major achievements over the past year or two include:
* Drafting and circulating the LDDI Resolution to over 120 groups. This is something we collectively developed over two or three months. If you're interested in finding out more and want to endorse the resolution, it's on the CHE website at www.healthandenvironment.org.
* Drafting a summary on neurotoxicants for lay audiences of the Centers for Disease Controls second biomonitoring report in 2003.
* Publishing five Practice Prevention columns on neurotoxicants for distribution in LDD groups’ newsletters and web sites.
* Exploring the development of a new sub-working group on criminal justice issues related to exposures to neurotoxicants. This is still very much in a formative phase.
* Fostering a new partnership with Pesticide Action Network of North America to figure out how we might partner on specific concerns like lindane and organophosphates.
* Drafting a letter to the Environmental Protection Agency's administrator Leavitt in regarding the regulations that would ease mercury emissions. Various groups in LDDI have signed on and we intend to do much more work on mercury in the coming months.
* Finally, planning our first major national meeting for LDD groups as well as interested researchers, health professionals, environmental health adovcacy organizations, and others to be held at the National Institutes of Health in Bethesda, MD on May 19th, 2004.
If you are interested in this meeting please contact Elise at emiller@iceh.org.
2. Science Update: Mercury in Regards to Autism Research: Martha Herbert, M.D., Ph.D., Pediatric Neurologist at Massachusetts General Hospital
I would like to preface this by saying I am not a specialist in mercury. I am a scientist concerned about toxins, mercury in particular. I am not a neurotoxicologist by trade.
"Autism, a Novel Form of Mercury Poisoning," published in Medical Hypotheses by Sallie Bernard, et al, was one of the papers that set off concern about a connection between mercury and autism. It took off from the 1999 call to remove Thimerosal from vaccines. This paper was a review of findings in multiple systems (immune, sensory, neurological, motor, behavioral) where mercury intoxication produced autism like symptoms and suggested that there could be a relationship; that this would be a novel, previously uncharacterized, form of mercury poisoning and that there would be predisposition to it. There was subsequently an Institute of Medicine hearing in July 2001. The conclusion was that there was insufficient evidence to support or reject this, but that it was a plausible hypothesis. Subsequent to that, there was a paper published in the Journal of Pediatrics, by Nelson and Doman(sp?), arguing that some of the points raised in the Bernard paper really were circumstantial and yet, some of the points in that paper were also circumstantial. For example, using acute poisonings in adults to refute a developmental mercurial syndrome. There's a response to that also in Medical Hypotheses. It was rejected by the Journal of Pediatrics even though the Pediatrics piece was a direct criticism of the people who responded to it.
There have been papers saying there is no impact of mercury or Thimerosal on autism from the vaccine safety data. This is a ground of contention with a recent Verstraten(sp?) paper going up against the arguments from the Geiers, saying that there's a substantial increase in relative risk and the recent paper by Madsen about Danish data are going up against the critique by Safe Minds saying that if you reanalyze the publicly available data, there's a substantial impact.
There were hearings last week in the Institute of Medicine. The morning session, which was epidemiological, gave the impression that there was no problem, but the afternoon session, which was clinical and lab research, gave the impression that there was a problem.
There are also issues of selective vulnerability. There's a hair study by Holmes-Blackthel(sp?), et al, showing that children with autism do not have a correlation of more mercury with more exposure but they do not excrete mercury in their hair and that suggests a possible mercury retention syndrome.
Mady Hornig has a paper on administering Thimerosal to mice with different genetic vulnerabilities. The mice with autoimmune problems have behaviors and brain changes similar to those in autism, which are worse in males. Mice without immune problems do not show these problems. The immunological problem seems to work both ways, because not only are mice, which are immunologically vulnerable, more affected by mercury, but mercury itself can enhance auto-immunity. There's a paper by Haveranisab(sp?) stating that and also a recent paper by Via(sp?) and Sildergeld, not related to Thimerosal, showing an increase in auto-immunity.
Finally, there are a number of papers showing changes in brain related tissues. Baskin(sp?) shows that Thimerosal can be associated with apoptosis. Richard Dieth has a very recent paper showing that Thimerosal at extremely low doses can inhibit insulin like growth factor 1 and methylation and methionine synthase. The methylation piece is quite interesting because some of the genetic data points to problems with methylation and autism and it would be quite interesting to have a convergence of genetic problems and toxicological problems on similar mechanisms. There's a paper showing impacts of Thimerosal on the cerebellar neurons in rats, showing that there seems to be a dose-dependent oxidative stress phenomenon, cytotoxicity and reduction of glutathione in the cells that's concentration dependent, requiring more ethyl mercury or Thimerosal, than methyl mercury would have been required. What you get is a sense that there are ways in which the neural system tissues may be particularly vulnerable and this vulnerability may be mediated by genetic vulnerability and immunologic vulnerability. This raises the question of what kind of research strategy would we really need to address this and can we really rely on just epidemiological data when we're dealing with substantial genetic individuality and variability.
Elise Miller: Last year we had a discussion group following a Partnership Call on autism and we will probably have another call of those particularly interested in autism in the next couple of months. If you are interested in joining this discussion please contact me at emiller@iceh.org.
3. Science Update: Organophosphates and the Impact on Neurodevelopment: David Wallinga, M.D., Senior Scientist, Institute for Agriculture and Trade Policy
I would like to highlight a couple of very recent studies on organophosphates that add to a substantial body of scientific information that will be coming out. I will also talk about some other information that won't necessarily be in the peer-reviewed literature, but is coming to the EPA through the regulatory process.
The organophosphates are a class of about 34 insecticides that are designed to act against insects by disrupting the nervous system. They do this by inhibiting an enzyme called acetylcholinesterase, which works on transmitters or signal molecules in the brain. These transmitters are not only found in insects, but in the human brain as well. The EPA targeted this class of chemicals for review in 1996 with the Food Quality Protection Act. So there's been a lot of scientific as well as regulatory interest in them. In the past it was thought that the most potent impact of these chemicals on the nervous system was through the disruption of acetylcholinesterase. But some of the most recent science is showing that they have direct impacts on the development of the nervous system that have nothing to do with this enzyme. In December 2003, in Environmental Health Perspectives, a paper by Myer, et al, (including Ted Slotkin at Duke, as a co-author) talked about some of these alternative pathways that dursban (or chlorpyrifos) appears to have in the development of the neurological system. This includes things like disruption of DNA synthesis, disruption of the transcription of certain genes involved in the differentiation of cells in the brain during development and the expression of neurotransmitters and the receptors on cells to those neurotransmitters and the developing brain. Basically, they hypothesized that one of the ways that this happens is through effects on cyclic AMP, which has a variety of influences including influences in the division of cells, the differentiation of cells, the growth of axones, and cell death. This is really significant because if these different mechanisms that have nothing to do with acetylcholinesterase, are important in the developing brain then they're totally ignored by the current regulation of these chemicals that have been on the market for 30-50 years. These are the most neurotoxic pesticides on the market.
The other study I wanted to mention is on Methylparathion, which is one of the most potent of these organophosphates. A couple of years ago a number of people in Mississippi and Ohio and other places in the south illegally applied Methylparathion indoors, predominantly in housing for poor people. Now scientists at the ATSDR have done an epidemiologic study of some of the children that were exposed and said, "exposed children had more difficulties with tasks involving short term memory and attention. Additionally the parents of the exposed children, reported that their children have more behavioral and motor-skill problems, than did parents of unexposed children. That was in the January 2004 issue of Environmental Health Perspectives. This buttresses the evolving science showing that the developmental effects from exposure to Methylparathion do appear to be greater as do the other organophosphates. What I continue to work on is the disconnect between the science and how the regulatory agencies have kind of overlooked it to date.
The EPA has, for four years, been calling in data of the toxicity of organophosphates to the developing brain, and it's a very slow process. But over the next eighteen months there should be about 20 new studies specifically looking at developmental effects of these insecticides.
4. A Model Program: LDA's Healthy Children Project: Jane Browning, Executive Director of the Learning Disabilities Association
The task of the Learning Disabilities Association is to take this kind of information to the street. Specifically, how do we take all of this scientific knowledge to the public and raise their consciousness about the dangers of environmental toxins and move them to take action towards protecting themselves and their families and to move their legislators towards greater regulation of exposures to environmental toxins.
I initially conceived of the Healthy Children Project as a community organizing effort that would produce a speaker's bureau that would go into schools and take this message to various audiences. We quickly learned that each of our affiliates who took on this project went galloping off in the direction that they were best suited to do. It has been something that has lived its own life in every community that we have visited. The John Merck Fund funded this project. We were invited to present a proposal to them through the initial meetings of the Learning and Developmental Disabilities Initiative.
The four project sites that we selected were in Washington State, where our LDA affiliate had a lot of experience in working with students in high schools and middle schools. In Western New York, where our LDA affiliate had actually sued the Housing and Urban Development Department (HUDD), for failure to enforce their own regulations of lead abatement in the urban housing in Buffalo. In LDA California, Jo Behm immediately went into coalition with other statewide environmental organizations and has successfully lobbied the California State legislature. I'm sure everyone is aware of California's recent ban on PBDEs and that was more or less a direct result of their collective efforts there. In Maine, LDA built an eight-organization Alliance for a Healthy Maine. Collectively they shepherded two bills through the state legislature in 2002 and another three bills in 2003. All were aimed at reducing mercury exposure in the environment there. LDA of Maine received their own small grant from the John Merck Fund to support those coalition efforts and they raised public consciousness about the effects of environmental toxins on brain development through exhibits at health fairs and other conferences around the state in addition to their legislative policy action. LDA of western New York immediately went into coalition with other groups around the state. Collectively they worked with the attorney general's office to initiate a research project that correlates incidents of childhood disability with known pollution sites throughout the state of New York. This project is still underway. They are also supporting statewide testing of all school children for lead levels. They also work with the healthy schools initiative in New York.
At the national level we hired a coordinator, Kathy Lawson, to keep all these people in contact with one another. Kathy is putting together an informative website www.healthychildrenproject.org that will launch on March 5. Kathy has worked with the USPIRG, Stop Pesticides Now and with the Coalition for Healthier Schools, signing onto the CHS position statement, which includes a section on neurotoxicants in schools. Kathy has testified before an EPA panel, being the only advocate in a room full of chemical industry representatives. She has worked locally, in Pittsburgh, with our Clean Water Action. She passed a Bad Actors Law through the county council. We've worked with the World Wildlife Federation on the Women's Environmental Health Bill, which is pending before the US Congress.
The Healthy Children Project is adding an additional 15 local project sites, in the coming month. One of those projects is the production of a videotape for use in pediatrician's offices, by the LDA of Iowa. We are working with the Heinz Endowments Environmental Health Program here in Pittsburgh to organize a regional CHE meeting in February 2005. The University of Pittsburgh Department of Early Childhood Evaluation and Planning has developed an evaluation model for the Healthy Children Project. We think this model has great potential for application to lots of different kinds of programs that are aimed at reducing human exposure to environmental toxins. We will be able to preview that at the LDDI meeting in May.
5. A Model Program: AAMR's New Collaborating for Action Project: Doreen Croser, Executive Director of the American Association on Mental Retardation
The American Association on Mental Retardation is very grateful to the John Merck Fund for providing some support so that we could become a partner in this initiative.
Six months ago AAMR hosted a national summit on pollution, toxic chemicals, and mental retardation. This was viewed as a groundbreaking event. The Johnson Foundation allowed us to use the Wingspread Conference Center to hold the meeting. There were 34 special invited representatives from the developmental disabilities/mental retardation network and representatives from the environmental health network. It was a very good event and people were excited about it. They came to recognize that there was a great deal of commonality between the mental retardation issues and the environmental health issues.
The purpose of this summit was to create a national blueprint for health promotion and disability prevention. We wanted to develop a plan that contributed to the broader national effort and was specific as to what the MRDD community could do to have a positive impact. We began by providing accurate data. Ted Schettler and other scientists from the environmental health community and from the MRDD community talked about the state of research. We established collaborative relationships. We developed a consensus statement and framed a national blueprint. This blueprint is a little behind schedule because we've had some disagreement on some of the scientific issues, but it is in final editing and will soon be available. It will be available both in print and on the website www.aamr.org. This blueprint will identify our partners, our next step, our common message and it will give people in the MRDD community information and specific steps that they can take to implement the project.
In addition, in the last several months, we have been giving presentations at the respective meetings. There's also going to be another plenary session coming up at the annual meeting for the AAMR convention. We have also collaborated on several other funding proposals to develop specific education and training materials to advance the effort. What we have found is that people in the MMRD community need specific information. They haven't begun to think about the problem in the way that is practical, as far as what they need to do in the group home, or the sheltered workshop. We're trying to develop some practical tools that will help them do that.
As of the moment, the Merck Fund has helped us to fund a project director position to move this effort forward. We are currently interviewing for this position. If anyone knows someone who might be interested, we would be deeply appreciative.
6. Why galvanizing the LDD sector is so important: Ruth Hennig, Executive Director of the John Merck Fund
The John Merck Fund (JMF) shares CHE's vision of working toward disease prevention by building an environmental health movement that's led by people that are directly affected or involved in the diseases and disabilities that have environmental connections. We began two years ago to support CHE at its inaugural event and we just renewed support for another two years. Most of the funding has been going to LDDI.
As you've been hearing from Jane and Doreen, we're complementing our grant to LDDI with support directly to LDD organizations like LDA and AAMR. Two years in, the strategy is meeting and succeeding beyond our expectations. As Elise said, the membership in LDDI is growing. These kind of leadership groups have the capability to develop active programs that are both incorporating environmental health into their educational materials for their members and other visitors to their websites, but also participating in federal and state level policy advocacy. In our view LDDI really does have the capability to be a model for other health and disease sectors or groups in becoming a force in the environmental health movement and helping move us all in the direction of disease prevention.
7. Questions and Answers:
Robert Verhoogen, M.D., Pediatrician and Professional Advisory Board, Learning Disabilities Association of California:
There's all this talk about Thimerosal in relation to autism, but has anyone looked in general at the effect of mercury that could be coming through either diet or the mother's diet or early fetal development, given what Ted Schettler has said in the past and what David Wallinga said today. In autism it seems that there's definitely a genetic vulnerability since there's such a relatively stereotypical pattern of presentation of the clinical picture. But with learning disabilities and attention disorders that's not at all as clear. Could it be that that very early developmental effect of mercury is there rather than looking at vaccines as the cause for autism?
Ted Schettler, M.D., M.P.H., Science Director, Science and Environmental Health Network:
The question is exactly right. There is a strong genetic component to autism and a genetic component to some of the other developmental disorders that probably is not quite as strong as it is for autism. There's a pretty good reason to believe why environmental factors are important in autism, because even in identical twins, there's not a 100% certainty that if one has autism the other will. The studies on that vary between 75 and 90% or 65 and 85%. It probably is a genetic predisposition and then an environmental component that contributes. The question is whether mercury might be a candidate for that. Thimerosal is one source of mercury that we've been intentionally giving to infants and that's why it came up. But there are other sources of mercury as well in our diet.
One of the issues that we have to confront is whether or not we're actually dealing with a heterogeneous group of conditions. There may be a subset of children with autism who actually do have something happen post-natally. As opposed to some other groups that are affected by some very early events. For example we know that the children who were exposed to thalidomide in-utero, had a much higher risk of autism. It appeared that the window of vulnerability was around twenty to twenty-five days of gestation. This actually may be a heterogeneous group of conditions and that's going to make this even more difficult to tease apart.
Martha Herbert: Don't necessarily assume that because the behavior seemed the same among these children that are all necessarily the same. There's a great deal of heterogeneity and it may be that the behaviors that look like they're all the same are a final common pathway for multiple diseases and a lot of people seem to think that. This is another way of supporting what Ted was just saying about heterogeneity.
Lin Nelson, Ph.D., Professor, Environmental Studies, Evergreen State College:
Could anyone talk more about legislative efforts and the response of legislators to these issues, particularly what kind of testimony has been most compelling and effective?
Jane Browning: I'll use LDA of Maine as an example, because they have been so active with the state legislature. They've taken a very educational approach. It's viewed as a long-term, ongoing effort that's not just around one particular bill. The coordinator of our group is a pretty well known activist in the state, so it's built on a layer of existing relationships. The testimony is not based solely on science, but relies heavily on the In Harm's Way report (from the Physician for Social responsibility of greater Boston) as our core text. This text has an array of very good presentations of the scientific material and conveys to legislators and every other member of the public the logic behind exposures and the outcomes. Of course mercury is an endocrine disrupter and its actions are very well documented and very well known. The greater effects of mercury have been the focus of all the main bills. The public is already conscious of the mercury levels in fish.
Ruth Hennig: Maine is one state that is willing to take leadership positions on a number of environmental health issues. Mercury is front and center on their radar screen. There have been a number of mercury related bills passed in the last two years. One thing that is clear in talking to the coalition coordinators and staffers of legislators, as well as the media, is how important it's been for groups like LDA and the Autism Society (whose primary identity and purpose is about public health and disease prevention) to be involved in getting those bills passed.
Neil Gendel, Project Director, Healthy Children Organizing Project, Consumer Action:
We do a lot of community-based education, especially with communities with English as a second language. I would very much look forward to seeing the fact sheets that you have been developing.
Jane Browning: The new website, www.healthychildrenproject.org, will be loaded with those kinds of materials.
Michael Lerner, Ph.D., President, Commonweal:
If you were on a radio or television show and asked, "What do you believe about the relationship between environmental contaminants and learning disabilities?" What would you say in that context?
Jane Browning: I would say that environmental toxins can be the triggers that turn on those genes that have a propensity for the cognitive impairment. There is no single gene that causes a learning disability by any means. There is a familial tendency towards learning disabilities and ADHD, but within a family one person will be affected while another won't. There are other factors that enter into the demonstration of learning disabilities. It's the combination of a genetic propensity with the environmental exposure that results in the expression of that learning disability. The reason that we think that environmental toxins are triggers is because of the rising incidents of learning disabilities and ADHD.
Doreen Croser: There is not a clear connection between mental retardation and environmental contaminants. We have not done nearly enough research. We know that alcohol contributes to cognitive disabilities and mental retardation. We know that mercury and lead are clear causes, but others, like pesticides, are less clear. We think that they contribute to the overall neurological functioning.
David Wallinga: One thing that came out of the Wingspread conference was a slightly different way of looking at the question. Are children with mental retardation or developmental disabilities at increased risk for further injury from environmental contamination and exposure? The point was raised that those populations aren't studied due to the concern about confounders, they are often excluded from a so-called, normal population.
Elise Miller: The shared LDD concern is that we don't really understand the relationship between, for example mercury exposure and health endpoints such as ADHD, as opposed to autism or mental retardation. The science isn't there yet. In other words, we can't say one organophosphate actually causes ADHD as opposed to autism. We don't know that and may never know that. What we can say, however, is that given what we do know in terms of the 12 neurotoxicants for which we have more extensive data is that there are widely used chemicals that seem to impair the development of the brain, starting in-utero going on through adolescence as the brain is still developing. Genes also come into play and maybe a greater influence on what kinds of symptoms manifest in some children more than others with other children. So there is that genetic component in combination with environmental exposures that is also very crucial. In addition, we know there are dozens if not 100s of suspected neurotoxicants that we have not started to study, nor have we researched how these chemicals may act in combination.
Another shared LDD concern is that there's still controversy around what we know in terms of the actual numbers of the children who are affected by LDDs. Because we haven't done a good job health tracking, we don't have solid baseline numbers. We also have a more formalized labeling and diagnosis system. That said, it is apparent to many people, particularly when you talk to parents and teachers and hear their stories, that there are greater and greater numbers. Regardless of the increases we may or may not be seeing, having one in six kids impacted by these disabilities and the fact that we could prevent many of the toxic environmental contributors to these disabilities is something we need to address as a society.
Nicole Rogers, MPH, RPCV, Special Projects Coordinator, Bureau of Environmental Health, San Antonio Metro Health District:
The EPA has recently expressed that the mercury levels in the blood of Inuit mothers and children would be considered hazardous waste if it was to be discarded. The children are showing some learning disabilities, but they're not showing a high rate of autism. Are there any studies out there that show the genetics across cultures? (Nobody knew of any studies.)
Elise Miller: Thank you to everyone who joined us on this call and particularly to the speakers.
