=======================Electronic Edition========================
RACHEL’S HAZARDOUS WASTE NEWS #364
—November 19, 1993—
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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DIOXIN AND PCBS LINKED TO ENDOMETRIOSIS
Endometriosis is a mysterious, painful disease that affects 6 to
9 million American women, according to estimates by the Mayo
Clinic.[1] Endometriosis occurs exclusively in species that
menstruate (humans and non-human primates). The disease occurs
when bits of the endometrium (the tissue that lines the uterus)
somehow escape the uterus and become implanted on other pelvic
organs. Usually the implants occur on the outside of the
ovaries, the fallopian tubes, the uterus or its supporting
muscles.
The mislocated cells imitate the menstrual cycle, first
thickening and then bleeding as menstruation begins. Because the
implants are embedded within other tissues, there is nowhere for
the blood to go. Blood blisters form, irritating the surrounding
tissue, which may create a cyst (sometimes also called a nodule,
tumor, lesion, implant, or growth) to encapsulate the blister.
The cyst, in turn, may become a scar or an adhesion (abnormal
tissue that binds organs together). Scars or adhesions on the
ovaries or fallopian tubes can prevent pregnancy.
Typical symptoms of endometriosis include chronic pain,
particularly pelvic pain; severe period pain; pain with sex;
infertility; painful bowel movements with the period; painful
urination or other urinary problems with the period and at other
times; chronic fatigue; chemical sensitivities and/or extensive
allergies and other allergic diseases; and, sometimes, autoimmune
diseases, including Hashimoto’s thyroiditis and lupus.
Endometriosis can run in families; it most commonly strikes women
between 25 and 49 but it can begin as early as 11. It generally
ends with menopause, though estrogen replacement therapy can
reactivate the disease.
Although more than 4500 research papers have been published on
endometriosis, the cause of the disease remains a mystery.
Now new thinking about endometriosis has been stimulated by
research linking dioxin exposure to the disease in rhesus
monkeys. In rhesus monkeys, endometriosis develops spontaneously
and resembles the human disease both anatomically and clinically.
In the rhesus, disease manifestations include growth of cysts
and adhesions involving the ovaries, ureters, colon, and urinary
bladder, just as in humans.
The recognition of dioxin as a contributor to the disease in
rhesus monkeys is considered an exciting breakthrough by
scientists who have been studying the disease for two decades or
more, unsuccessfully seeking a cause.
The new research reveals a clear dose-response relationship
between low levels of dioxin in the diet and development of
endometriosis in rhesus monkeys. The more dioxin, the worse the
endometriosis, according to experiments conducted at University
of Wisconsin and reported this month by Sherry E. Rier and
co-workers in the journal, FUNDAMENTAL AND APPLIED TOXICOLOGY.[2]
A colony of 24 wild [feral] female rhesus monkeys 6 to 10 years
of age was obtained in 1977. From 1977 to 1983 the animals were
housed at the University of Wisconsin’s Biotron; from 1983 to the
present, the animals have been housed at the Harlow Primate Lab
in Madison, Wisc. In 1977, the monkeys were randomly assigned to
3 groups of 8 animals each. Control animals were not exposed to
dioxin, animals in the low-dose group were exposed to 5 parts per
trillion (ppt) in their diet and monkeys in the high-dose group
were exposed to 25 parts per trillion. Dioxin was administered
in the animals’ feed for 5 years, from 1977 to 1982. The point
of the original research was to see if low doses of dioxin in the
diet interfered with reproduction in the rhesus colony.
The dioxin connection to endometriosis was discovered almost by
accident. As the researchers themselves wrote, “This study was
originally undertaken 15 years ago to investigate the long-term
reproductive effects of exposure to dioxin in the rhesus monkey.
Twelve years after the initiation of this work, [in 1989], a
dioxin-exposed animal died and was noted at autopsy to exhibit
widespread endometriosis. In 1990 and 1992, two additional
dioxin-treated animals died of severe infiltrating endometriosis.
During this time, we became aware that these animals and others
in the colony displayed symptoms similar to human disease at the
onset of menses, including anorexia [diminished appetite;
aversion to food] and behavior consistent with pain. In view of
these findings, the present study was performed to document
endometriosis in this unique colony of monkeys and to determine
whether the severity of the disease was correlated with exposure
to dioxin.”
This new study describes the 17 live monkeys currently remaining
in the colony, plus the 3 monkeys that died of extensive
endometriosis and were evaluated at autopsy.
The 17 living monkeys underwent laparoscopy in 1992. Laparoscopy
is surgery performed under general anesthesia. A small incision
is made in the abdomen, and a thin optical tube is inserted, so
that the animal’s internal organs can be observed and
photographed. In humans, as in monkeys, laparoscopy is the only
sure way to diagnose endometriosis because some forms of cancer
create the same symptoms.
Among the 20 monkeys, the presence and severity of endometriosis
was determined according to human criteria, using the revised
American Fertility Society (rAFS) system, which is universally
accepted. The rAFS system classifies the severity of
endometriosis according to number, size and placement of
endometriotic implants and the presence of adhesions. There are 4
stages of the disease: minimal, mild, moderate, and severe.
Among the rhesus monkeys, the incidence of disease directly
correlated with dioxin exposure. Endometriosis was present in
71% of the animals treated with 5 ppt dioxin, and in 86% of
animals treated with 25 ppt. This compares to 33% of the animals
exhibiting disease in the control group.
The severity of the disease was also correlated with the dose of
dioxin. According to the severity classification system, control
animals not exposed to dioxin exhibited either no disease (4 of 6
animals) or minimal disease (2 of 6 animals). Animals treated
with 5 ppt dioxin had no disease (2 of 7 animals), mild disease
(1 of 7 animals) or moderate-to-severe disease (3 of 7 animals).
Among the animals dosed with 25 ppt, 5 of 7 animals had
moderate-to-severe disease and only one was disease-free.
The authors conclude, “The results of these studies demonstrate
that chronic exposure to the chemical toxicant dioxin is directly
correlated with an increased incidence in the development of
endometriosis in rhesus monkeys. As determined by [standardized]
scoring systems, stage II [mild], III [moderate], and IV [severe]
disease were exclusively found in animals exposed to either 5 or
25 ppt dioxin. Furthermore, the severity of disease, as
reflected by the [standardized severity] score, was positively
correlated with the daily and cumulative dose of dioxin
administered.”
The reproductive history of these particular monkeys had
previously been reported. Reproductive function of mothers
exposed to 5 ppt was not significantly different from the control
group. Seven of eight females bred after 7 months of exposure to
5 ppt dioxin were able to conceive; 6 of these females gave birth
to viable infants and one gave birth to a stillborn infant. In
contrast, among the moneys dosed with 25 ppt, only 5 could
conceive and of these only one gave birth to a viable infant;
there were 3 spontaneous abortions and one infant died shortly
after birth.
These data suggest that maternal exposure to dioxin before and
during pregnancy can result in fetal mortality without overt
toxic effects on the mother. Humans in industrial countries now
eat an average of 133 picograms [trillionths of a gram] of
dioxins each day, 90 percent of it in fish, meat and dairy
products, according to the World Health Organization.[3] A 1992
study from Germany revealed that endometriosis is correlated with
the presence of PCBs in humans,[4] thus confirming findings first
reported in 1985 linking PCBs to endometriosis in rhesus
monkeys.[5] PCBs and dioxin both interfere with the immune
system and with the endocrine system (the body’s chemical control
system made up of endocrine glands, which produce hormones).
Researchers have suspected for some time that endometriosis is
somehow caused by malfunction of both the immune and endocrine
systems.
Dr. Audrey Cummings with U.S. Environmental Protection Agency is
now conducting laboratory research to see if dioxin exposure
causes endometriosis-like changes in rats.
Dioxin and PCBs are not the only potential culprits. As Dr. Theo
Colborn has recently shown, at least 45 chemicals widely
distributed in the environment, including 35 pesticides and 10
industrial chemicals, are now thought to damage or impair the
endocrine systems of fish, birds and mammals, including humans.[6]
For further information on endometriosis, contact: The
Endometriosis Association, 8585 North 76th Place, Milwaukee, WI
53223. Fax: (414) 355-6065. Families affected by the disease
can call the Association’s toll free line: 1-800-992-3636 for a
free packet of information.
–Peter Montague, Ph.D.
===============
[1] David E. Larson, editor, MAYO CLINIC FAMILY HEALTH BOOK
(N.Y.: William Morrow, 1990), pgs. 1101-1102.
Descriptor terms: endometriosis; msc; immune system; endocrine
system; allergies; lupus; hashimoto’s thyroiditis; rhesus
monkeys; studies; laboratory research; university of wisconsin
biotron; harlow primate lab; laparoscopy; audrey cummings; epa;
theo colborn; pesticides;