RACHEL's Hazardous Waste News #264

=======================Electronic Edition========================

RACHEL’S HAZARDOUS WASTE NEWS #264
—December 18, 1991—
News and resources for environmental justice.
——
Environmental Research Foundation
P.O. Box 5036, Annapolis, MD 21403
Fax (410) 263-8944; Internet: erf@igc.apc.org
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THE WINGSPREAD STATEMENT–PART 2:
MAJOR CHALLENGE TO ‘BUSINESS AS USUAL’

An international group of 21 scientists[1] met at Wingspread in
Racine, Wisconsin in July, 1991 to discuss evidence that
chemicals in the environment are causing changes in the sexual
development of wildlife and conceivably in humans as well. (See
RHWN #263.) The group produced a five-page “consensus statement.”

Sexual development in wildlife, as in humans, is controlled by
the endocrine system, a group of organs, tissues and cells that
secrete hormones; the hormones interact with other cells,
initiating chemical/biological reactions with far-reaching
consequences. Male hormones are called androgens; female hormones
are called estrogens.

It is now known that some chemicals disrupt the endocrine system.
The Wingspread statement identifies the following: “Chemicals
known to disrupt the endocrine system include: DDT and its
degradation products [DDE and DDD], DEHP
(di(2-ethylhexyl)phthalate), dicofol, HCB (hexachlorobenzene),
kelthane, kepone, lindane and other hexachlorocyclohexane
congeners [forms], methoxychlor, octachlorostyrene, synthetic
pyrethroids, triazine herbicides, EBDC fungicides, certain PCB
congeners [forms], 2,3,7,8-TCDD and other dioxins, 2,3,7,8-TCDF
and other furans, cadmium, lead, mercury, tributyltin and other
organo-tin compounds, alkyl phenols (non-biodegradable detergents
and anti-oxidants present in modified polystyrene and PVCs),
styrene dimers and trimers, soy products, and laboratory animal
and pet food products.”

In animals, and in humans, sexual characteristics are established
at a particular point during development in the womb or egg. For
example, Dr. Theodora Colborn of the World Wildlife Fund
(Washington, DC) points out that a single dose of dioxin,
administered to a pregnant rat at day 15 of the pregnancy–near
the time when gender is established–results in demasculinization
and feminization of male offspring.[2]

Samples of herring gulls from Lake Ontario collected in 1975 and
1976 showed cellular and anatomical changes in embryos and in
newly hatched chicks that caused feminization of male chicks and
overdevelopment of female reproductive organs. Elevated
concentrations of DDE [a break down by product of DDT] and other
residues were found in eggs from the same population. To test
whether these sexual problems might be linked to the presence of
the DDT, laboratory experiments were conducted in which Western
gull eggs were injected with concentrations of DDT similar to
those found in the Great Lakes environment. Male chicks became
feminized, developing ovarian tissue and oviducts.[3]

What is becoming clear is that the older picture of chemical
toxicity underestimates the number and kinds of effects that
chemicals can have in fish, birds, and mammals. For decades, U.S.
regulatory officials have focused their attention almost
exclusively on cancer. Meanwhile, many of the chemicals that
have been dumped into the environment, and are now coursing
through food chains, cause many other detrimental effects besides
cancer.

For example pesticides such as DDE, dieldrin, lindane, mirex,
toxaphene, and PCBs, block communication between cells. Normal
metabolism [energy use] and development of a cell may be
disrupted because movement of nutrients, electrolytes, and
hormones in and out of a cell is blocked by the presence of these
poisons.[4]

Furans, benzo[a]pyrene, 2,3,7,8-TCDD [dioxin], DDE, dieldrin, HCB
[hexachlorobenzene], lindane [beta-HCH], mirex, toxaphene, and
PCBs induce enzyme activity. [Enzymes are large protein molecules
that promote chemical activity in the body; the presence of
particular enzymes makes possible particular chemical reactions
that would not otherwise be possible.] When the enzyme activity
is induced, normal products of the endocrine hormonal system can
be released into the bloodstream. This can disrupt the role of
steroid hormones, affecting growth and sexual maturation.[4]

The structure of DDT and DDE are, themselves, quite similar to
estrogens and thus may mimic female hormones. In addition, DDE
induces enzymes that break down male hormones. Under different
circumstances, dioxin acts like an estrogen, or it may act as an
anti-estrogen (what causes the same chemical to have opposite
effects is not understood).[4]

At one Superfund site where data are available, humans are
experiencing abnormalities of sexual development. At the Brio
site south of Houston, Texas, where a housing development was
built atop a chemical dump, girls 4 to 5 years old have developed
pubic hair and enlarged breasts. One child (now four years old)
was born without any genital organs; chromosome tests revealed
that this is a male child, though he has a birth canal. This
information, and other data about abnormal sexual development of
children at the Brio site, is contained in a unique database of
information that resulted from a health survey of the community
by a local group (HELP) and by the Environmental Health Network
(EHN) in Harvey, Louisiana.[5] Such surveys–providing an
unusually valuable source of information about health problems
near chemical dumps–are under way in several Superfund
communities, looking for patterns of problems, including the
kinds the Wingspread statement warns of.

The Wingspread statement presents a major new challenge to
advocates of “business as usual.” The participants in the
conference represent 17 different fields of scientific inquiry.
They have many thousands of data points on which they have based
their conclusions. If they are right, we are all being exposed,
on a daily basis, to chemicals that threaten out reproductive
health, and the health of our offspring.

Because hormones and hormone disrupters do their work at
extremely low concentrations, the only “safe” dose of an
endocrine-system disrupter is zero. Thus any new sources of these
chemicals should be aggressively discouraged while we figure out
how to minimize exposure to the quantities of these chemicals
already in the environment.
–Peter Montague, Ph.D.

===============
[1] Participants in the Wingspread meeting included the following
individuals (whose institutional affiliations are given for
identification purposes only): Dr. Howard A. Bern, Professor of
Integrative Biology (emeritus) and Research Endocrinologist,
University of California-Berkeley; Dr. Phyllis Blair, Professor
of Immunology, University of California-Berkeley; Sophie
Brasseur, Marine Biologist, Research Institute for Nature
Management, Texel, The Netherlands; Dr. Theo Colborn, Senior
Fellow, World Wildlife Fund, Washington, DC; Dr. Gerald R. Cunha,
Developmental Biologist, University of California-San Francisco;
Dr. William Davis, Research Ecologist, Environmental Research
Laboratory, U.S. Environmental Protection Agency, Sabine Island,
FL; Dr. Klaus D. Dohler, Director, Research, Development &
Production, Phar-ma Bissendorf Peptide GmbH, Hannover, Germany;
Glen Fox, Contaminants Evaluator, National Wildlife Research
Center, Environment Canada, Quebec, Canada; Dr. Michael Fry,
Research Faculty, Department of Avian Sciences, University of
California-Davis; Dr. Earl Gray, Section Chief, Developmental
and Reproductive Toxicology Division, Health Effects Research
Laboratory, U.S. Environmental Protection Agency, Research
Triangle Park, NC; Dr. Richard Green, Professor of Psychiatry in
Residence, School of Medicine, University of California-Los
Angeles; Dr. Melissa Hines, Assistant Professor in Residence,
School of Medicine, University of California-Los Angeles; Timothy
J. Kubiak, U.S. Fish and Wildlife Service, East Lansing, MI; Dr.
John McLachlan, Director, Division of Intramural Research,
National Institute of Environmental Health Sciences, Research
Triangle Park, NC; Dr. J.P. Myers, Director, W. Alton Jones
Foundation, Charlottesville, VA; Dr. Richard E. Peterson,
Professor of Toxicology and Pharmacology, School of Pharmacy,
University of Wisconsin-Madison; Dr. P.J.H. Reijnders, Head,
Section of Marine Mammology, Research Institute for Nature
Management, Texel, The Netherlands; Dr. Ana Soto, Associate
Professor, Tufts University School of Medicine, Boston, MA; Dr.
Glen Van Der Kraak; Assistant Professor, University of Guelph,
Ontario, Canada; Dr. Frederick vom Saal, Professor, Division of
Biological Sciences, University of Missouri-Columbia; Dr. Pat
Whitten, Assistant Professor, Department of Anthropology, Emory
University, Atlanta, GA.

[2] David J. Hanson, “Dioxin Toxicity: New Studies Prompt Debate,
Regulatory Action,” C&EN [CHEMICAL & ENGINEERING NEWS] August 12,
1991, pg. 13.

[3] Theodora E. Colborn and others, GREAT LAKES GREAT LEGACY?
(Washington, DC: Conservation Foundation, 1990), pg. 139.

[4] Theodora E. Colborn and others, cited above, pg. 142.

[5] For more information about the Brio site, contact HELP: 10904
Scarsdale Boulevard, M263, Houston, TX 77089; phone (713)
992-1867. For advice about health surveys, contact Linda King,
Environmental Health Network, P.O. Box 1628, Harvey, LA 70058;
phone (504) 362-6574.

Descriptor terms: endocrine disruptors; racine; wi; wildlife;
sexual development; endocrine system; fish; birds; herring gulls;
mammals; humans; reproductive hazards; reproductive disorders;
ddt; des; pesticides; herbicides; insecticides; fungicides;
theodora colborn; wwf; superfund; brio; ehn; environmental health
network;

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