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.