Stephen Safe and Kavit Ramamoorthy are toxicologists at Texas A & M University.
Are environmental pollutants the real culprit in declines in male fertility and
increases in breast cancer? The jury is still out.
Some researchers maintain that certain chemicals, in particular those that
mimic the body's natural hormone estrogen, may be implicated in declines in
male fertility and increases in testicular and prostate cancer in men and
breast cancer in women. However, recent research fails to establish a firm link
between endocrine disrupting hormones and these observed effects.
While it's not possible to study human beings the way we study rats, an
inadvertent experiment was conducted in the 1940s, 50s, and 60s on pregnant
women who took the drug DES, a synthetic hormone taken to prevent miscarriage.
Their children suffered a host of health problems, including a rare form of
vaginal cancer in women and deformed genitalia in men.
Since DES is a potent synthetic estrogen, some researchers have leapt to the
conclusion that environmental contaminants that mimic estrogen and chemicals
such as dioxins and PCBs represent a significant toxic risk to humans.
However, the complicated mechanisms that governs the endocrine system are still
poorly understood. Therefore, there is reason to proceed with caution in
blaming environmental contaminants for these effects. In fact, new research as
well as new analysis of old data reveal conflicting results. For example, a
review of 61 reports published between 1938 and 1991 revealed that mean sperm
counts decreased by nearly half, and that seminal volume also decreased by more
than a third between 1940 and 1990. However, studies conducted in Toulouse,
France and Seattle, Washington, show no decrease in sperm counts in donors at
fertility clinics between 1972 and 1993. And studies in Denmark also show that
semen quantity and quality did not decline between 1922 and 1972.
Additional studies show significant geographical variations in sperm quality
that cannot be readily ascribed to environmental contamination. Studies
conducted in New York, Minnesota, and California confirm wide geographic
variations in sperm concentrations. These results were echoed in similar
studies conducted in France and Denmark.
Other factors cloud the sperm count studies. For example, a report published in
the journal Human Reproduction showed that the process of self-selection can
skew the results of the studies conducted. In that report, D.J. Handelsman
concludes that it is invalid to extrapolate the sperm output of self-selected
volunteers to the general male community.
Moreover, additional studies attempting to correlate levels of the metabolite
DDE in human breast milk a good indicator of exposure of the general population
to the pesticide DDT to testicular cancer in men were inconclusive. While DDE
levels were similar in all Scandinavian countries for the past 30 years, there
was a remarkably higher incidence in testicular cancer in Denmark than in
Finland, where the rates of the disease were low. Moreover, as testicular
cancer incidence has been steadily increasing, DDE levels have decreased 80 to
90 percent in Scandinavia and most Western countries since the mid-1970s.
Initial studies reporting higher levels of DDE and PCBs in breast cancer
patients than in controls were not corroborated in four large studies on breast
cancer patients in Europe, Mexico City, and the United States. A critical
examination of all the evidence, then, produces mixed results.
People are exposed to a number of natural estrogens throughout their lives. It
is well known that lifetime exposure to estrogens naturally produced by the
endocrine system significantly increases the risk for breast cancer in women.
Women who reach menarche at an early age, postpone childbearing, or reach
menopause later are at greater risk due to the increased exposure to estrogen.
In addition, the foods we eat contain both natural estrogenic and
antiestrogenic compounds that further complicate an accurate assessment of
the role of exogenous toxins.
In short, researchers need more time to pinpoint the exact mechanism that
triggers adverse health effects in humans, interpret the conflicting evidence
of epidemiological studies, and understand the complex interaction of the
suspected chemicals and other unidentified culprits, whether natural or
external. Until then, claims that hormone-mimicking chemicals are responsible
for reported declines in sperm counts and increases in cancers in both men and
women are unproven, the authors maintain.
Safe and Ramamoorthy's article "Disruptive Behavior: Endocrine Disruptors,
Sperm Counts, and Breast Cancer" will appear in the Fall 1998 issue of FORUM
for Applied Research and Public Policy.