Fact
Sheets
Issue:
Environmental chemicals may play a role in the development and progression
of endometriosis.
Background:
Endometriosis is an estrogen dependent disease in which cells
that line the uterus (endometrial cells) begin to grow in the pelvis
and abdomen, most commonly on the ovaries, the outer surface of the
uterus, the intestines or the ligaments that support the uterus. It
is estimated that this disease affects approximately 15 % of women
of reproductive ages. Women with endometriosis experience pain on
menstruation and intercourse often leading to time off work, medication
and in many cases surgery. The cause of endometriosis remains undetermined.
Disease trends: There is very little known concerning changes
in the frequency of this disease. For example, it is not known if
there are more women with endometriosis today than in previous years.
In addition, it is not known if women living in regions with high
exposure to environmental chemicals are at greater risk for developing
this disease.
Consistency of the data: A small number of hospital-based studies
have been conducted in which the association between endometriosis
and exposure to polychlorinated biphenyls (PCBs) and dioxin (TCDD)
have been investigated. While two studies have reported a positive
association between exposure to these chemicals and endometriosis
the other two studies were unable to find a relationship. Unfortunately
the number of patients included in theses studies was too small to
generate convincing evidence either in support of or against an association
between endometriosis and environmental chemicals.
Experimental evidence: In rhesus monkeys long term exposure to
TCDD in the diet has been shown to be associated with an increased
frequency and severity of spontaneous endometriosis. Analysis of the
serum from these monkeys revealed an association between endometriosis
and exposure to TCDD and PCBs that act through the same receptor as
TCDD. However, a second rhesus monkey study with long-term exposure
to a commercial PCB mixture failed to find any relationship between
this mixture of chemicals and endometriosis. A third study involving
Cynomolgus monkeys showed that dioxin treatment at low doses antagonized
the growth of endometrial cells whereas higher doses increased the
survival and growth of these cells.
In both rats and mice environmental chemicals such as the pesticide
methoxychlor as well as PCBs and TCDD have been shown to facilitate
the survival and growth of endometrial cells. These studies show that
estrogenic chemicals can act to promote the growth of endometrial
cells placed in the abdomen of these animals. A recent study has demonstrated
that TCDD can antagonize the growth inhibiting effects of progesterone
on endometrial cells growing outside of the uterus.
Biological plausibility: While both the human and animal data
are inconclusive, the animal data show that environmental chemicals
can affect the growth of endometrial cells albeit at high concentrations
compared to the levels measured in tissues of the general population.
However, it is not known if these chemicals are acting like hormones
or are antagonizing the effects of the body's hormones through non-endocrine
mechanisms.
Conclusion: Taken together the data do not support a conclusion
that environmental chemicals are playing a role in the development
or progression of endometriosis. The evidence does support however
a conclusion that environmental chemicals may play a role in the pathology
of this disease.