CHE Partner Forum: Call for Ideas and Comments

Dear CHE Partners,

We want your ideas! We’re in the process of evaluating various aspects of CHE’s services and initiatives and generating potential new ones. Given we are indeed a collaborative partnership, your innovative suggestions as to what CHE might do (within our mission, below) to address gaps or needs you see in the environmental health field would be genuinely welcome.

To facilitate this, we’re opening this Partner Idea Forum, a platform where you can offer your ideas. This one is interactive in that you can see, respond to and build on other partners’ suggestions.

As a major learning community for the field, CHE wants to do even more to serve our partners around the world. Please take a few to submit your thoughts. We’ve pulled some comments from recent surveys and posted them below to start the conversation, but feel free to start a new topic.

As with all comments to this blog, civil and respectful dialogue is expected. Please identify yourself as you submit comments. If you prefer to submit private comments that won’t be shared on this blog, please send them to us at

Note this Partner Idea Forum will stay open only until December 15th, so please get your ideas in soon!


The Collaborative on Health and the Environment’s (CHE’s) primary mission is to strengthen the science dialogue on environmental factors impacting human health and to facilitate collaborative, multifactorial, prevention-oriented efforts to address environmental health concerns. Founded in 2002 as a program of Commonweal, CHE is an international partnership of almost 5000 individuals and organizations in 87 countries and all 50 US states, including scientists, health professionals, health-affected groups, nongovernmental organizations and other concerned citizens, committed to improving human health across the lifespan.

CHE’s primary activities include:

  1. Sharing emerging scientific research on various  environmental factors that can contribute to disease and disability;
  2. Fostering interdisciplinary and inclusive collaboration among diverse constituencies interested in those links; and
  3. Facilitating effective actions to improve health across the lifespan.

CHE is nonpartisan and does not endorse specific policies. Anyone sharing CHE’s mission and supporting its Consensus Statement is invited to become a CHE Partner.

CHE has created graphical representations of the scope and structure of our work, shown at right and below (click on the graphics for larger versions).

CHE Administrative Graphic

A Story of Health: Something for Everyone

written by Elise Miller, MEd

We all know there are multiple contributors to health and disease, but let’s say you want to figure out what the latest science says on environmental links to, say, asthma? Or learning disabilities? Or childhood leukemia? Pretty daunting, isn’t it? Which websites have the most evidence-based science? Which articles are accessible without paying a subscription or membership fee? What do those research findings mean for your patients, your family, and community? And many other pressing questions. Most health care professionals can’t begin to keep up with the emerging scientific literature, much less the rest of us.

cover of A Story of HealthFortunately, A Story of Health is a brilliant, innovative new resource that can help you find out how various environments interact with our genes to influence health across the lifespan. Based on the latest peer-reviewed research, it’s more than a bunch of scientific facts thrown together with fancy graphics. It’s a story, or really—multiple, interactive, and interconnected stories that touch us and teach us not only about risk factors for disease, but how to prevent disease and promote health and resilience.

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The Effect of Environmental Chemicals on Insulin Production: Implications for All Types of Diabetes

Sarah Howard
Coordinator of CHE’s Diabetes-Obesity Spectrum Working Group

In a recent review, published in the leading diabetes journal Diabetologia, Hectors et al. (2011) describe how numerous environmental chemicals affect the insulin-producing beta cells of the pancreas. These effects, the authors argue, may be significant in the development of type 2 diabetes. Chemicals like bisphenol A, PCBs, dioxin, organophosphorous pesticides, arsenic, heavy metals, and others, can all affect how the beta cells function, and can interfere with their capacity to secrete insulin.

In type 2 diabetes, both insulin resistance—the body’s inability to respond correctly to insulin—and beta cell malfunction contribute to the disease. The inability of the beta cells to produce enough insulin leads to high blood glucose levels, and eventually diabetes (in many people with type 2, insulin production is higher than normal, to compensate for the insulin resistance—but it is still inadequate to bring blood glucose under control).   

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Get a Grip on Toxic Chemicals

Reps. Doyle and Murphy are well positioned to help protect us

Maureen Swanson
CHE Partner and Director of the Healthy Children Project for the Learning Disabilities Association of America

This letter was originally published in the Pittsburgh Post-Gazette. It’s republished here with the author’s permission.

Imagine all the chemicals used in televisions, computers, upholstery, car seats, building materials, even children’s pajamas. Imagine that some of these chemicals migrate from products into dust and dirt, and build up in our bodies. They are found in the cord blood of newborns and in breast milk. Imagine that these chemicals are similar in structure to the notorious PCBs – carcinogens banned from use in the late 1970s.

Now wouldn’t you also imagine that these chemicals were tested and found to be safe to human health before they were allowed into our products and homes?

Unfortunately, that is not the case.

Polybrominated diphyenyl ethers are flame retardant chemicals that persist in the environment and build up in the food chain and in people. Laboratory studies link exposure to PBDEs with lowered IQ and attention problems. This summer, a study of pregnant women found that those with higher levels of PBDEs had reduced levels of thyroid hormone, which is essential to a baby’s brain development.

But despite growing scientific evidence linking toxic chemical exposures to serious disease and disability, our government does not require that PBDEs – or any of the other 80,000 chemicals on the market – be tested for effects on human health.

That could be about to change, and two Pittsburgh members of Congress are in key positions to help make it happen.

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Brain Tumour Risk in Relation to Mobile Telephone Use: Results of the INTERPHONE International Case–control Study

Stelios A Zinelis
CHE Partner

The Interphone Study Group (2010)1 conducted a study on mobile telephone use has made this conclusion:

“Overall, no increase in risk of glioma or meningioma was observed with the use of mobile phones. There were suggestions of an increased risk of glioma at the highest exposure levels, but biases and errors prevent a causal interpretation.”

This study was completed in 2004, but for unknown reasons, the results were  published six years later, upon demand by scientific organisations such as the European Environment Agency and the European Union (2009)2 (which partially funded the study, along with the International Union against Cancer [Mobile Manufacturers Forum and GSM Association]),  who were concerned about the effects of mobile phone use on public health.

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Dioxin – Scientific Analysis

This letter is reprinted with permission from the Environmental Working Group, a CHE partner. See the original letter with full science analysis on EWG’s website.  

Dr. Timothy Buckley, Chair
Dioxin Review Panel
Science Advisory Board
Environmental Protection Agency (EPA)
Washington, DC

Dear Dr. Buckley,

Twenty-five years after publishing its first assessment of dioxin, a common industrial pollutant and food contaminant, the Environmental Protection Agency (EPA) has yet to establish a safe daily dose for human exposure to this potent chemical.

Dioxin (2,3,7,8-Tetrachlorodibenzo-p-dioxin, also known as 2,3,7,8-TCDD, or TCDD) may well be one of the most-studied of all chemical pollutants. The U.S. National Toxicology Program has listed dioxin as a known human carcinogen since 2001 (NTP 2005), and the U.S. Environmental Protection Agency has proposed to do the same (EPA 2010a). There is a large and persuasive body of research dating from the 1950s showing that dioxin undermines fetal development, damages the reproductive and immune systems and causes severe skin ailments and other disorders.

As U.S. industrial data demonstrate, dioxin is released from municipal waste incinerators; industrial and military hazardous waste treatment facilities; pesticide manufacturing and paper bleaching plants; and a wide range of other industrial processes. In the 1970s, dioxin was identified as a contaminant in Agent Orange, the notorious defoliant deployed by the U.S. during the Vietnam War and blamed for diabetes and other diseases among exposed personnel (Chamie 2008; Cranmer 2000; Gupta 2006).

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Letter to Michelle Obama

March 25, 2010 

First Lady Michelle Obama
The White House
1600 Pennsylvania Avenue NW
Washington, DC 20500

Dear Mrs. Obama:
We, the undersigned, are partners in the Collaborative on Health and the Environment, an international network of scientists, health professionals and advocates committed to using the best available science to improve the health of our families and our communities. We are deeply grateful for your leadership in facing the challenge of the obesity epidemic, which has concerned many of us for years. We also strongly support the initiatives that you are undertaking to address this major public health issue, which is having such a devastating effect on the health of American families.

We would like to underscore in this letter that the obesity epidemic is the result of many interacting factors and not just a lifestyle challenge—something that you acknowledge, but is rarely highlighted in the media or understood by the general public. The Institute of Medicine (IOM), for example, has publicly stated the importance of access to healthy food to help curb the increasing prevalence of obesity.[1] Along these lines, it is clear the federal government, given its ability to influence food production through subsidies, needs to incorporate strategies to promote more healthful and less calorie-dense, nutrient-poor food.

Other factors contributing to obesity include socioeconomic status and genetic predisposition, as well as poorly designed communities that discourage walking and biking.

In addition to these issues, the prestigious international Endocrine Society published a seminal report last year stating that, “scientific research implies the impact of environmental substances in the generative roots of obesity.”[2] The rapidly growing body of scientific evidence suggests that chemicals known as endocrine disruptors may be associated with a range of health concerns, including various cancers, developmental disabilities and infertility. In addition, some of these chemicals may also act as “obesogens” – that is, substances that trigger the propensity to develop obesity. Of critical importance, these obesogens appear to reprogram metabolism starting before birth, thereby increasing a child’s predisposition for obesity before he/she is even born. In addition, research shows that these chemicals may also promote the development and maturation of fat cells throughout life. In other words, we cannot ignore the evidence that these chemicals, found in everyday products and in our food and water, may also contribute to this epidemic.

The science on obesogens is very clear in animal studies (please see the attached article in press for the San Francisco Medical Society Journal [available on CHE’s website]). Although we have little information yet about how obesogens impact humans, there is some initial research in humans suggesting the urgent need for further study.[3]

The truth is that we as a society need to recognize all the interacting factors that can contribute to obesity—including the risk that exposures to obesogens can pose. Any campaign that does not take into account the role of these chemicals in the obesity epidemic will run counter to President Obama’s promise that this administration will be guided by the best available science. Given this, the emerging science clearly indicates that national chemical policy reform is an essential ingredient of your campaign against childhood obesity.

We congratulate you on your foresightedness in choosing obesity as one of your signature issues as First Lady. Please know we would also be happy to discuss ways to address the full range of concerns associated with obesity and to work with you and your colleagues to champion prevention as essential to real health care reform for all Americans.

Thank you again for your leadership and consideration.

With best wishes,

Bruce Blumberg, PhD, Professor, Departments of Developmental and Cell Biology and Pharmaceutical Sciences, University of California, Irvine

Susan Braun, Executive Director, Commonweal

Linda C. Guidice, MD, PhD, MSc, Professor and Chair, Department of Obstetrics, Gynecology and Reproductive Science, The Robert B. Jaffe, MD Endowed Professor in the Reproductive Sciences, Director, Center for Research on Origins and Biological Consequences of Human Infertility, Director UCSF Women’s Reproductive Health Research Career Development Center, University of California, San Francisco

Andrea Gore, PhD, Gustavus and Louise Pfeiffer Professor, Division of Pharmacology and Toxicology, The University of Texas, Austin

Richard J. Jackson, MD, MPH, Chair and Professor, Environmental Health Sciences, School of Public Health, University of California, Los Angeles

Phil Landrigan, MD, MSc, Ethel H. Wise Professor and Chairman, Department of Preventive Medicine, Professor of Pediatrics and Director of the Center for Children’s Health and the Environment, Mount Sinai School of Medicine

Philip R. Lee, MD, Former United States Assistant Secretary of Health, Chancellor of the University of California at San Francisco, Professor at Stanford University

Michael Lerner, PhD, President, Commonweal

Elise Miller, MEd, Director, Collaborative on Health and the Environment

John Peterson Myers, PhD, Founder, CEO and Chief Scientist of Environmental Health Sciences

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

Carlos Sonnenschein, MD, Professor, Department of Anatomy and Cellular Biology, Tufts University School of Medicine

Ana Soto, MD, Professor, Department of Anatomy and Cellular Biology, Tufts University School of Medicine

R. Thomas Zoeller, PhD, Chair and Professor, Biology Department, Morrill Science Center

[1] Institute of Medicine reports: The Public Health Effects of Food Deserts. Workshop Summary, Local Government Actions to Prevent Childhood Obesity and Progress in Preventing Childhood Obesity: Focus on Industry—Brief Summary: Institute of Medicine Regional Symposium. Available on the IOM website,, viewed March 11, 2010.

[2] Diamanti-Kandarakis E et al. Endocrine-disrupting chemicals: An Endocrine Society Scientific Statement. Endocr Rev. 2009 Jun;30(4):293-342. Available online at, viewed March 11, 2010.

[3] Grün F, Blumberg B. Endocrine disrupters as obesogens. Mol Cell Endocrinol. 2009 May 25;304(1-2):19-29. Heindel JJ, vom Saal FS. Role of nutrition and environmental endocrine disrupting chemicals during the perinatal period on the aetiology of obesity. Mol Cell Endocrinol. 2009 May 25;304(1-2):90-6.