The Paris Appeal: Calling Attention to the Role of Environmental Contaminants in Cancer

July 29, 2004
3:32 pm US Eastern Time

Call Transcripts

1. Welcome:  Call Moderator:  Steve Heilig, M.P.H., Co-Director of CHE, Director of Public Health & Education, San Francisco Medical Society

We always start these calls with a science update of breaking news or evolving concepts. Pete Myers is generally the person we call on for this because he is so well known in this arena and so broadly knowledgeable. Those of you who have been on these calls before know this and are probably aware of his relatively new news service at  http://www.environmentalhealthnews.org/, which tracks environmental health science and media reports from around the world. He’s also co-author of Our Stolen Future and has a website there as well: http://www.ourstolenfuture.org/. He is one of the core CHE scientists developing and updating our science website: http://www.healthandenvironment.org/. So, Dr. Myers, will you please tell us something new today?

2. Science Update: Pete Myers, Ph.D., CEO, Environmental Health Sciences, Co-Author, Our Stolen Future

Thank you, Steve. I would like to draw your attention to a potentially very important paper that’s just gone online last week at Environmental Health Perspectives, which is the journal of the National Institute of Environmental Health Sciences. It’s an epidemiological study of asthma in children. Those of you who follow asthma science know that there’s a lot of understanding of environmental agents that trigger asthma attacks. But there’s much less understanding of what factors are underpinning the overall increase in asthma itself. The general sense is that something is increasing sensitivity to triggers, so that while the triggers themselves may not have increased, and some have appeared to decrease, the incidence of asthma itself is increasing because of something that’s causing sensitivity.

Several ideas have gotten a lot of attention with research over the past couple of years, including exposure to diesel exhaust and even some theories about improved infant health care and increased cleanliness, which is proposed to lead to a poorly trained and hypersensitized immune system, which leads to asthma. These new data show a strong relationship between certain phthalates and three childhood allergic conditions: asthma, rhinitis and eczema. It’s a large case-control study which was done in Sweden. They measured phthalate levels in dust in children’s bedrooms and compared the dust levels with kids with these allergic conditions and controls. They found a two- to threefold increase in the cases versus the controls. The results were highly significant.

DEHP, one type of phthalate, was linked to asthma, while BDZP was linked to rhinitis and eczema. The overall odds ratios were statistically significant and they also showed a very clear dose-response curve.

Now, for me, one of the most fascinating parts of this was that they point out that the results are consistent with a model of phthalate interference with a control of immune system sensitivity, which is a model actually published in 1997. The model proposed that a metabolite, a breakdown product of DEHP called MEHP, mimics a certain type of hormone called prostaglandin that are important in setting immune system sensitivity. The theory in this model is that MEHP turns on genes that prostaglandins turn on. That leads to heightened respiratory track sensitivity, exactly the sort of process that would contribute the rise in asthma.

This remains a theory. Its plausibility is really enhanced by these new epidemiological data. The authors of the new study point out in their publication in EHP that phthalate exposure is virtually ubiquitous and that it has increased in home indoor air over the same time period in which the asthma epidemic has been rising. To me, frankly it sounds a lot more plausible than the so-called hygiene hypothesis.

You can read about this new work on http://www.healthandenvironment.org/. You’ll find links there to the original study. If you’re having difficulty finding it, go to: http://www.environmentalhealthnews.org/, it’s the top item in the center column. Thank you.

3. Featured Presentations:

Steve Heilig: Thank you Pete. We’re going to move to our featured presentations now. For an introduction, I’ll say that this has been an interesting call to put together. We’ve been doing these calls for quite some time and a number of people have asked when we might do one on general issues in cancer. It’s something we have discussions about because it is a subject of a lot of controversy. Cancer and the environment is something that a lot of good people disagree about as well. So there’s what you might call internal controversy among people who are involved in environmental health. In talking with the general public, when you talk about environmental contaminants and health, the first response is often  "oh yeah, cancer." There was, in fact, a number one song in the 1980's by a guy named Joe Jackson that was titled Everything Gives You Cancer. We now know that that's what some hypochondriacs believe, on one hand, but on the other hand, there are those who say that nothing can give you cancer, short of tobacco smoke -- if they even concede that.

I heard a talk the other day at Stanford University by Shanna Swan, who laid out some very interesting concepts in epidemiology that point to new ways of looking at this. We have asked one of our core scientists, Ted Schettler, to frame what these new issues are and how we should look at these various environmental factors and how they are linked to cancer.

* Ted Schettler, MD, MPH, Science Director, Science and Environmental Health Network

Thanks very much, Steve. I want to begin by simply talking about some of the problems with addressing this issue. Studying and understanding the causes of cancer is really a complex topic for a number of interconnected reasons. First, cancer biology itself is complex. Cancer is initiated and then promoted through a series of stages before a clinical disease becomes apparent. The latency period between initiation and clinical disease may be decades long, varying somewhat with a specific tumor type. Long latency periods make it difficult to study events or circumstances that may contribute to cancer incidence. Whether or not the process will progress from initiation through promotion to clinical disease depends on a number of factors, including immune system status, adequacy of cell repair mechanisms, defective cell growth regulation and so on.

Second, the causes of cancer are numerous and interrelated. The general categories include, of course, genetic and environmental influences. Within the environmental category, the factors are diet, tobacco and alcohol use, exposure to industrial chemicals and environmental contaminants more generally, radiation and infectious agents. Dietary variables include total caloric intake; anticarcinogenic substances in food; carcinogens that occur naturally in foods, or that are introduced in food production, storage, or preparation; carcinogenic pesticides; aflatoxin and nitrosamines are examples of the latter.

Beyond diet, carcinogenic industrial chemicals and environmental contaminants can be encountered in the home, work place or community. They are in air, drinking water and food. Occupational exposures in workers are often but not always higher than in the general population. Studies of workers are the source of much of the information of cancer risk associated with the exposure to a variety of chemicals. What these studies tell us about cancer risks in the general population is a matter of considerable debate. Large well-designed twin and sibling studies conclude that environmental factors are more important than genetic factors for virtually all cancers, even those where there is a significant genetic component. Moreover, immigration studies conclude that for many cancers, cancer risk is largely established early in life. People who emigrate to another country before age 20 tend to acquire cancer risk patterns of the country they move to, whereas people who emigrate after age 20 tend to retain the cancer risk pattern of the country they move from. This suggests not only that environmental factors are important risk determinants, but also that early-life events matter significantly. To the extent that prenatal, childhood, and pubertal events contribute to determining cancer risk later in life, one can see how this becomes extremely difficult to study because of the long latent period before the appearance of clinical disease.

More than 20 years ago, Doll and Peto published a still widely quoted paper on the causes of cancer deaths in the U.S., in which they estimated that occupational exposures and general environmental pollution were relatively small contributors to cancer mortality. They estimated that dietary variations were responsible for about 35% of cancer mortality and tobacco use for about 30%. Their estimates were based chiefly on epidemiologic evidence since they concluded that animal and other laboratory studies could not provide reliable human risk assessments.

Since then epidemiologic study techniques have had to be revised in order to reflect improved understanding of cancer biology. For example, we now know that gene/environment interactions play an important role. Not all people in a population are at equal risks from exposure to carcinogenic substances. Then they had genetically determined metabolic pathways that detoxify substances differently, affecting cancer risk. Or they may have differing hormone patterns with differing responses to hormone disrupting chemicals.

Prenatal events increasingly appear to play an important role. For example, in animal tests, maternal nutrition during pregnancy can strikingly increase cancer risk in offspring when they are exposed to a carcinogen later in adulthood. This is an instance of intergenerational nutritional interactions with toxic chemicals, where relatively small prenatal exposures to chemicals that influence tissue differentiation, for example dioxin, influence susceptibility to chemical carcinogenesis later in life.

So, in summary, interactions between diet and exposure to carcinogens and other substances that influence cell growth and differentiation, along with radiation, infectious agents and genetic factors during periods of susceptibility or vulnerability, increasingly seem to be important determinants of cancer risk. Separating these factors as individual determinants of risk may serve some purposes, but to insist on that practice exclusively does not reflect current understanding of cancer biology. These interactions make the design of epidemiologic investigations more complex, but studies that reflect an understanding of these interactions are much more likely to be fruitful.

On the Protecting Our Health website, we have some summary papers on specific cancer types that further discuss these issues in case you're interested.

 Steve Heilig: Thank you very much, Ted. I'd also like to mention the link to Chemical Contaminants and Human Disease: A Summary of Evidence, the matrix that Ted and others put together, which is an extensive document that lays out evidence on specific diseases and toxicants.

The impetus for doing this call at this time was a statement that was issued recently called The Paris Appeal, which can be found at http://www.artac.info/static.php?op=AppelPremPage.txt&npds=1%22. This is a striking document, not only because of what it says, but also because of who signed onto it, a lot of leading scientists, some Nobel Prize winners, some of the renowned figures in environmental epidemiology. It has some very strong statements in it such as:

"Whereas chemical pollution in all its forms has become one of the main causes of current human scourges such as: cancer, infertility, congenital diseases, etc."

It also makes some strong recommendations for remedying this.

One of the people who was involved in the signing and issuing of this document was Dr. Richard Clapp, and we are very pleased to have him with us today. He is going to give us some background information on how the document came about.

* Richard Clapp, MPH, DSc, Professor, Department of Environmental Health, Boston University, School of Public Health

Thank you Steve. I'm going to try to cover a lot and don't have the time to do it justice. I'd like to add one thing to something Ted just said, the Doll and Peto article, which appeared in 1981, keeps getting recycled. In addition to the limitations that Ted mentioned, it was an evaluation of the mortality experience of white people in the U.S. under the age of 65. So it didn't really address the full scope of cancer and cancer mortality in that it limited it to white people and we have more than white people in this country and in this world. Also many of childhood cancers are not big causes of death, and yet incidences are increasing. So, that's a bit more of what's missing from the Doll and Peto analysis.

I want to do two things. I want to talk a little bit about the epidemiologic trends of cancer in the U.S. and then I want to talk about the Paris Appeal. Because I think that is the reason why we had the Paris Appeal in the first place.

Cancer is one of the diseases that strikes fear into the heart of everybody. I think it's the one that people fear most. There are surveys, at least in the U.S., that try to get at what disease is the most fearsome in the minds of the public and cancer usually comes out number one.

The fact is that although cancer mortality has begun to come down in the last decade, cancer incidence is not coming down. Periodically, there are statements from, for example, Health and Human Services or the National Cancer Institute, saying that we may have turned the corner, or we may have begun to conquer cancer, or the war on cancer may have been victorious. I think these are premature declarations of victory and that the victory doesn't mean that people aren't getting cancer in great numbers. It may mean that they aren't dying at as high a rate as they have in the past. They still live with cancer and their families are still suffering the burden of having the disease and having to pay for care or all the psychological impacts that go with that.

So some of the recent trends about cancer in the U.S. that I would like to highlight are that overall cancer incidence is either flat or for some types of cancer it is going up and for other types of cancer is going down. But the overall picture is not one of comfort or victory. Liver cancer is actually one of the cancers that is going up most rapidly. In this country it is a rare form of cancer, it's seen relatively rarely compared to other types of cancer. In the rest of the world liver cancer is much more common. In Africa and Asia, for example, it's closely linked to the hepatitis virus and aflatoxin exposure. Whereas, in this country, I think the reason that liver cancer is increasing recently has to do with the Hepatitis A epidemic. Although that's probably the one that leads the list as the one that's increasing most rapidly, it's not one that we would associate with environmental contaminants; it is, nevertheless something to watch carefully.

Non-Hodgkin's lymphoma is another type of cancer that, at least until recently, has been increasing rapidly in this country and in other parts of the world. Non-Hodgkin's lymphoma is directly linked to environmental chemical contaminants such as solvents, trichlorethylene and perchloroethylene in particular, and pesticides. Farmers, for example, who are exposed to those pesticides are at increased risk of getting Non-Hodgkin's lymphoma. Recently that seems to have begun to taper off. I think, about a year ago, Protecting Our Health had an article from Leonard Hardell and co-authors from Sweden, that suggests that the leveling off of Non-Hodgkin's lymphoma in Sweden may be because of banning a certain pesticide and the lack of exposure to those pesticides after the banning. If that's true, I don't know if we can say that in this country yet, but if that's true, I think that's an example of how primary prevention may work. When you no longer expose people to the substances that cause cancer, sure enough, the rates of that cancer begin to come down.

Another type of cancer that's worrisome is melanoma of the skin. Mostly everyone has accepted that this seems to be due to ultra violet light exposure. Again, that's increased in the last two to three decades because of the thinning of the protective stratospheric ozone layer. As you all know this was caused by the chlorofluorocarbons making their way up into the upper atmosphere. Because we've banned chlorofluorocarbons, that pattern of increasing melanoma of the skin and even non-melanoma of the skin may begin to decrease sometime into the next century.

The good news in all this cancer incidence data is lung and oral cancer are both going down, especially in males. I think the bulk of the cause of lung and oral cancer is cigarette smoke, both mainstream and sidestream. So, if we prevent exposure, then those rates should come down and it looks like we are beginning to see that.

Childhood cancer, as I already mentioned, is not coming down. The rates of childhood cancer are actually going up in this country. That can't be due to lifestyles such as whether you smoke cigarettes or even where you work. It's also not due to changing genetic composition, because human gene pools don't change that rapidly due to increased rates of childhood cancer as we've seen in the last couple of decades.

So those are some very broad trends. Ted spoke about the complexities of all this, and how epidemiologic studies trying to sort out those complexities are extremely difficult, time consuming and expensive to do. So, we're left with that. We're watching these broad trends and we don't have the details about what might be the causes of some of these trends. There's a lot of research taking place right now that might elucidate that further.

In the meantime, the Paris Appeal comes before us. It was actually an anticancer group in Paris, whose acronym is ARTAC, who developed it. The head of it is Dominique Belpomme. I heard him speak and then met him a few times and spoke with him before this conference. Dominique Belpomme is an oncologist who's tired of pumping chemotherapeutic agents into people once they've already gotten cancer, and wants to focus his attention on how to prevent cancer in the first place, which is to say, prevent carcinogenic exposures. Rather than how to screen people so that they can get treatment, but how to intervene at a point where people don't even need to be screened. Primary prevention is what that's called. He strikes me as an honest scientist and oncologist who's looking at the world around him and who's come to the conclusion that we've got to do something more drastic in order to prevent this devastating disease.

Belpomme was the convener of this conference which was held in Paris on May 7, and from which the Paris Appeal was released. You've probably all seen it, but you can access it through the ARTAC website or you can download a PDF. It contains a lot of whereas' and a lot of articles and it refers to a lot of international treaties, but what it all boils down to, is that we've got to prevent exposure to carcinogenic substances. The last item, measure number seven, is to support the REACH (Registration Evaluation and Authorization of Chemicals) Initiative. This conference, which had about 600 people at the UNESCO office in Paris, was really an attempt to build support for REACH. There were members of the European Parliament who attended who talked about the status of the REACH Initiative and different politics in different countries. They talked about the role of the U.S. in trying to undermine REACH, the U.S. government role, one speaker in particular named Colin Powell, and U.S. corporate lobbyist roles in approaching EU members of parliament to try to convince them not to vote, as a parliamentary matter, to endorse REACH. So you can imagine what this conference was like. There were 600 people in one room with everyone from organic farmers to organizations such as Greenpeace to Nobel Prize winners. I was on a panel with Luc Montaignier. He is one of the co-discoverers of the HIV virus. Oncologists and epidemiologists from throughout the EU and especially from Paris were there. So it was a broad gathering of folks. It was very energized. It went on all day and into the evening. There were lots of people chatting at breaks and tabling outside, giving people literature and so forth. It was a very vibrant exercise and I think it was really focused on REACH, but has a lot to tell us in this country about what we need to be doing as well.

Steve Heilig: Thank you. Next we have Dr. Stephen Thomas joining us to share his thoughts on some of the previous comments and to give us some information on what he’s been working on.

* Stephen B. Thomas, PhD, FAAHB, Director, Center for Minority Health, Philip Hallen Professor of Community Health and Social Justice, Graduate School of Public Health, University of Pittsburgh

Our efforts at the University of Pittsburgh Center for Minority Health are focused solely on the elimination of ethnic and racial disparities in health care, and cancer being one of the seven priority areas that we focus on. We do that by building infrastructures in African American neighborhoods. Trusted community partnerships, we believe are essential for the translation of scientific breakthroughs, many of which have been talked about in this conversation, to actual steps people can and should take to reduce their risk for, in this case, cancer. So, I'll limit my discussion to one of our major concerns as it relates to health disparities in cancer and that is breast cancer in African American women and the fact that African American women are discovered with advanced tumors at much younger ages. As you know the prevalence of breast cancer is higher in white women and yet the prevalence of mortality from breast cancer is much higher in black women.

My question to you has to do with some of the modifiable environmental components that may be involved in the presence of aggressive breast cancer tumors in African American women at much younger ages. From my reading of literature on this issue and from some of the speculation that might be occurring has to do with the role that estrogens play in aggressive growth of tumors, and estrogen just being one of several factors associated with aggressive tumors. My question has to do with to what extent are environmental triggers for aggressive tumors prevalent in African American communities and what message should be communicated to the African American communities as it relates to exposure to these environmental triggers. What role does exposure to potentially toxic hair care products, for example, play in triggering cancers or stimulating their aggressiveness? To what extent does race, even the social construction, play in understanding the cancer disparity in breast cancer that we see?

So those are a few of my questions, because our work here lies at the intersection of translating what we know from science into what people can do in their neighborhoods and their communities and their everyday lives to reduce their risks to chronic diseases like cancer.

4. Questions and Answers, Comments, Discussion:

Steve Heilig: Would any of our previous speakers like to address any of the questions that Dr. Thomas just raised?

Ted Schettler: I would like to add to the discussion about breast cancer that there is a similar sort of disparity in prostate cancer, where African American men have a higher incidence and more aggressive disease. There's a fair amount of discussion about the role that early detection plays and so forth. All of this is summarized in the paper at http://www.healthandenvironment.org/, for those of you who are interested.

Stephen Thomas: The Institute of Medicine's Report, The Unequal Burden of Cancer, discussed the problem and laid out the epidemiology and proposed a number of possible ways in which to frame solutions. One of the discussions had to do with the issue of race and the fact that it has no biological basis and is a social construction and therefore how do we use race as a variable in our research. I'm curious, in terms of the environmental arena, to what extent this whole discussion about race and ethnicity has shaped the language, the nomenclature that we use to talk about these health disparities.

Richard Clapp: I would like to throw in an example from Pittsburgh, which was coke oven emissions and their ability to cause lung cancer. I think it was Carol Redmund who was the first author of a series of studies who looked at this in the Pittsburgh steel workers. I think there wasn't really a racial susceptibility to coke oven emissions on the tissue of African American men's lungs. It was just that they got the worst jobs. They were the topside workers, the ones with the biggest exposures. So racism, in that sense, played into the exposures are greater, because the people who were put in the way, so to speak, of those exposures were politically and economically disenfranchised in the steel industry. So, that's how it played in. It wasn't that there was some genetic susceptibility, it was who got the exposures and why.

Stephen Thomas: Philosophically, that's exactly how we, at the center, approach these issues, in the sense that African Americans and other disadvantaged populations may well be like the canary in the mine. However, there are other parts of the scientific community that may not take the same perspective. I'm wondering, for example with breast cancer, this notion that tumors in black women are more aggressive because of something about black women.

Vincent Garry, MD, DABT, Director Environmental Medicine, University of Minnesota Medical School: Has anyone ever mentioned the possibility of looking at it as polymorphisms, for example, the estrogen receptor, among different groups of people?

Richard Clapp: Right now there are four NIEHS breast cancer and environment research centers that are set up and funded. I was on a call with someone from NIEHS who said that there would be a conference on the status of their work coming in November of this year. I think the question you just asked is being addressed by at least one of these four centers. Perhaps we should have a second call after that, or have someone from one of those centers present.

Julia G. Brody, PhD, Executive Director, Silent Spring Institute: I'm not completely up-to-date on this, but Nancy Kreger has been proposing that the gap between African American and white breast cancers is going away.

Pete Myers: One of the things that's coming clear out of the animal research is that in-utero exposure can alter receptor density. It's very complicated at this moment, given how little data we actually have to try and tease apart the types of questions that are being addressed. But the issue of in-utero receptor density setting is going to emerge as a central issue in a lot of things that we're working on.

Karen Florini, Senior Attorney, Environmental Defense: I want to thank all the speakers and particularly the follow-up with Ted Schettler. That was a very nice summary and critique of the Doll and Peto Study. Dr. Clapp added some additional helpful points as well. Has this been written up in a one-pager, because it's something that gets thrown in our faces every time we turn around. It would be very nice to have a succinct write-up, specifically of its limitations.

Ted Schettler: I have not done that and I don't know that anyone else has, but I do agree that there's a need for it. I think that as follow up to this call and CHE's work to the general topic of cancer, this is the kind of thing that would be useful as we move ahead and look at this topic more comprehensively.

Vincent Garry: Has anyone looked at pancreatic cancer, which is greatly increasing, and the possible environmental origins of that?

Lovell Jones, PhD, The University of Texas at Houston, Center for Research on Minority Health: I just came from a workshop with a presentation by Dr. Fatima Jackson, who indicated that there are relationships with sassafras and the use of different ingredients that, along the Mississippi Delta area, have been associated with an increase in pancreatic cancer. There may be other environmental factors that may be similar. I don't know of anyone else looking at that though.

When I was involved in writing the report for the Institute of Medicine on environmental justice, there were three elements that I stated that were needed to really look at the issue of cancer. Not only cancer in persons of color, but in the underserved as well. The first, that's been a recurring theme, at least here in Houston, is the issue of data and accurate data. The other is in regards to scientific studies that involve the affected population, both at the beginning, the middle, and at the end, because we don't do that now. We really don't have the data we need in terms of scientific information. The earlier data I was talking about was more in terms of demographic, but in terms of scientific information, we're behind the eight ball as well. The last is when one has to use the precautionary principle in involving populations, especially those that have the least access and are disenfranchised, during epidemiological studies where we want to find the problem, but we don't provide access to solve the problem. In my mind this is just repeating the Tuskegee Study. I think what I'm pointing to is both data and accuracy in terms of history and I think that will go a long way in addressing health disparities.

Stephen Thomas: Thank you Dr. Jones. In terms of the Tuskegee Study, it is indeed the paradigm case and for many African Americans, it is the one they can make reference to in terms of why they don't trust the system, in terms of access and care. But I think it is important to point out that on May 16, 1997, President Bill Clinton issued a formal apology to, at the time, eight of the remaining survivors. Those survivors accepted that apology. To me this is an opportunity to aggressively talk about ways of moving forward, with the legacy of the Tuskegee Study in mind informing how we do this. I think it's really important to be moving towards atonement. An apology means, "I'm sorry," by a president who wasn't even alive in 1932 when the study started. We do need to talk about atonement and that means making things better. So I'm really interested in how we translate what the science is telling us into actionable steps to be taken in communities. We opened up with the asthma research in Sweden. Can we act on that in ways that address exposure to these toxins in homes, or do we need to now replicate that in Pittsburgh? We need more of that translated action, because the burden of disease in these communities is so great. There is a legitimate resistance to being involved in more studies that are observational in nature and not remediation in nature. We need very specific consensus around where we can act, based on what we know.

Lovell Jones: I agree with you wholeheartedly, however, as Tip O'Neil said, all politics being local, I think all health is local. That was one of the things that I said to Senator Specter in getting him to provide the funds for The Unequal Burden of Cancer. When we were talking about the issue of data, I told him that the data he referenced in a lot of his speeches were data that did not come from Pennsylvania, it came from a lot of other sources and that there was not a registry in state, nor was that information utilized, in terms of some of the national reports that had been coming out at that time. Our project in Houston focuses on prevention and doing the prevention and the treatment all in the course of the project that we're launching. So it addresses a community need in terms of the health care, but it also gets at trying to figure out what the real problems are in terms of contributing to their health. Is it the same in regards to the causal factors or is it a different set of causal factors? One of the statements that was made here was, "research and science tends to always be focusing on the symptoms and not the causation." So we're trying to get more to the causation.

Mark Mitchell, MD, MPH, President, Connecticut Coalition for Environmental Justice: I'm a member of the National Environmentalists Advisory Committee, health and research subcommittee. One of the things that we're looking at is vulnerability and how to define vulnerability, particularly with environmental triggers that may be associated with illness. I think we're very early in the science, particularly with cancer. I did have a question about what's known about current levels of radiation and cancer.

Stephen Thomas: If you go to the Intercultural Cancer Council website, one of the governing board members, on the faculty at the University of Hawaii, is from Palau. The reason why I mention him is that Palau and that area of the Pacific Ocean has cancer rates that are about 60% higher than the rates that are sited in the U.S. They think that a lot of it is attributed to radiation and they're focusing a lot of their work along those lines. So, I often say, the people who are working directly on the problem often have more information than the people working theoretically on the problem.

Philip R. Lee, MD, Chair, Collaborative on Health and the Environment, Professor Emeritus of Social Medicine, UCSF, UCSF and the Institute for Health Policy Studies, Stanford University, Program in Human Biology: This has to do primarily with what both Dr. Jones and Dr. Thomas were saying about what you do in the community. I'd like to add two things. One is the studies that Dr. Lasker and her group at the New York Academy of Medicine and the Center for Collaborative Studies and Health are doing, called the Pathways Project. They've got about eight community groups out of 700 that are working on collaborations that work and these are in various different parts of the country. The key factor is involving the people in the community who are affected by the problem, in defining the problem and then developing some solutions. You might call it participatory democracy instead of representative democracy at that level. Some of these partnerships are very different from the top-down, kind of CDC-directed, so called partnerships, where you're a partner if you do what they say. These are coming in the opposite direction. They have an article in the Journal of Urban Health, and they've now got a website on their Pathways Project.

The second is California's Proposition 10, where the tobacco tax money set up programs for projects; they have countywide collaborations and then they have specific projects. I heard about one yesterday, on lead poisoning, where you can only go so far where you focus on the lead in the paint and cleaning up the house. What they did in a small-scale study with 90 families is a complete collaboration with the family, engaged the family in the process and apparently the results have been dramatic. So, again it's about engaging the people with the problem in solving the problem. That's one of the things that we don't do in public health. We tell people what to do and we need to take almost the opposite approach to what we've been doing and what we've been trained to do in public health.

Stephen Thomas: Agreeing with all that you've just said with regard to implementation strategies, my point at this level, where here in Pittsburgh, we actually have engaged the community, is that we still must be scientifically sound.

Philip R. Lee: There's no question about that. But then you need to have the scientists work with the community, instead of just telling the community what they have to do.

Stephen Thomas: My point has to do with, where do we have consensus for acting? Like the Sweden study, if I heard Dr. Jones right, the Sweden study is fine, but we might have to do a case-control in Pittsburgh here as well. When we're challenged with limited resources that's where the balancing act comes in. The absence of consensus or the real or perceived sense of confusion in the scientific community as new studies come out sometimes can stymie the efforts at the local level. And keep in mind that the funders, including foundations and others, want to have some assurance that what we're doing and what we're investing in is evidence-based and the most efficacious.

Steve Heilig: This is one of our ongoing themes—there's always more research needed, but when does action start? I wanted to ask Michael Lerner, one of the founders of CHE and the author of Choices in Healing, a guide to complimentary approaches to cancer, to talk briefly about follow-up to this discussion.

Michael Lerner, PhD, President, Commonweal: Thank you Steve. I particularly want to express my appreciation to Dr. Jones and the entire conversation in the second part of this call. Environmental justice issues in cancer is a very provocative conversation, which the Collaborative on Health and the Environment is committed to continuing. I also want to say that we believe that there is sufficient interest within the 900 CHE Partners to start a discussion or working group focused on cancer, just as we have one on learning and developmental disabilities and we have one on infertility.

I'd like to add a couple of key points. It's a matter of public record that the Susan G. Komen Breast Cancer Fund, which heretofore has not been very active on this, has commissioned a major review paper from Julia Brody and her colleagues at Silent Spring on environmental factors in breast cancer. This is a major turning point for the Komen Foundation and we believe that other major national cancer organizations will hear the concerns of their constituencies as well. Komen has made a very important decision to explore this issue and to think carefully and hard about how to proceed. I'm very impressed by the level of commitment I've seen within Komen to begin to think about this.

We feel that the time is right for the Collaborative on Health and the Environment to have a national dialogue among partners and scientists and concerned organizations and individuals, on the broader issues of cancer, going beyond just breast cancer, which has been the focus of many. So we would like to invite any of you on this call, and we'll put it out to all CHE Partners, who would like to participate in this discussion group. You would be most welcome.

Our goal will be focused on thinking about how to assess the science more broadly than it's being assessed now. We want to look at individual cancers, epidemiological studies, cancer biology, occupational cancers, cancer clusters, and the ineffective use of cancer registries. We want to review the Doll and Peto Study and the critique of it. We want to look at the disease interactions between conditions like obesity or DES or endometriosis and cancer, as well as veterinary cancers; the cancers in pets are very interesting because pets often have exposures similar to our own. Pete Myers' very important database and Theo Colburn's database will be invaluable. We also want to look at the issue of risk assessment and low-dose exposures, and so on. There are quite a number of topics that could be revisited, very much including the unequal burden of cancer, environmental justice issues, poverty and cancer and so forth. So our approach would be a portfolio approach, in which we'd be trying to identify the best thinking in each of these areas and make it accessible via the CHE websites and our conference calls to interested CHE Partners and others.

So if you are interested please be in touch with Frieda Nixdorf at info@healthandenvironment.org, saying that you'd be interested in being included in the announcements and calls on this. We welcome your interest.