Male reproductive health has deteriorated in many countries during the last few decades. In the 1990s, declining semen quality has been reported from Belgium, Denmark, France, and Great Britain. The incidence of testicular cancer has increased during the same time. Incidences of hypospadias and cryptorchidism also appear to be increasing. Similar reproductive problems occur in many wildlife species. There are marked geographic differences in the prevalence of male reproductive disorders. While the reasons for these differences are currently unknown, both clinical and laboratory research suggest that the adverse changes may be inter-related and have a common origin in fetal life or childhood. Exposure of the male fetus to supranormal levels of estrogens, such as diethlylstilbestrol, can result in the above-mentioned reproductive defects. The growing number of reports demonstrating that common environmental contaminants and natural factors possess estrogenic activity presents the working hypothesis that the adverse trends in male reproductive health may be, at least in part, associated with exposure to estrogenic or other hormonally active (e.g., antiandrogenic) environmental chemicals during fetal and childhood development. An extensive research program is needed to understand the extent of the problem, its underlying etiology, and the development of a strategy for prevention and intervention. Environ Health Perspect 104(Suppl 4): 741-803 (1996)

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Wild alligators exposed to persistent organochlorine contaminants, municipal waste compounds, and contemporary-use herbicides exhibit reproductive alterations that are thought to be caused by endocrine disruption. This study tests the hypothesis that these alterations, at least in part, result from exposure of alligator embryos to contemporary-use herbicides. Alligator eggs were collected early in development, exposed to estradiol-17β, atrazine, or 2,4-D (at dosages of 0.14, 1.4, and 14 ppm, plus a dosage of 0.014 ppm for estradiol-17β only) before the period of gonadal differentiation, and incubated at a temperature that would produce either 100% males or 100% females. Analysis of histology was performed on the gonads and reproductive tracts of hatchlings. In females, epithelial cell height of the Müllerian duct and medullary regression of the ovary were assessed, whereas in males, sex-cord diameter was measured. Eggs incubated at the female-determining temperature produced all female hatchlings, whereas the estradiol-17β treatments caused the production of females at the male-determining temperature. Neither atrazine nor 2,4-D had this effect. Both Müllerian duct epithelial cell height and medullary regression were increased in estradiol-treated animals, but no differences were noted between herbicide-treated alligators and controls. A previous study found that male alligators exposed to 14 ppm atrazine had elevated gonadal aromatase activity, but there was no difference in sex-cord diameter in this or any other treatment group. Additionally, we observed that hepatic aromatase activity was not altered by in ovo exposure to any of the treatments. These results indicate that these herbicides alone are not responsible for the gonadal abnormalities previously reported for juvenile alligators from Lake Apopka and emphasize the importance of anlyzing both the function ( i.e., steroidogenic enzyme activity) and the structure ( i.e., histological analysis) of the reproductive system. Structural assessment alone may be insufficient for detecting subtle endocrine alterations.

Xenobiotic compounds introduced into the environment by human activity have been shown to adversely affect the endocrine system of wildlife. Various species exhibit abnormalities of (1) plasma sex steroid hormones, (2) altered steroid synthesis form the gonad in vitro and (3) altered steroidogenic enzyme function. These endpoints are sensitive and relatively easy to measure quantitatively with reliability and precision. These observations have led to the conclusion that sex steroid hormones could be markers of exposure to, and altered function from, endocrine disrupting contaminants (EDCs). However, there are serious limitations in the use of steroid hormones as generalized markers of EDC exposure. Steroid hormones exhibit seasonal, ontogenetic, gender and species-specific variation. Moreover, the regulation of sex steroid plasma concentrations is a relatively complex phenomenon capable of shorterm (minutes — hours) alteration due to environmental inputs, such as acute stress -- an activational response. Alterations in steroid synthesis and degradation also can be a response to altered embryonic development due to EDC exposure — an organizational response. If steroid hormones are to be used as biomarkers, then closely controlled, well designed sampling has to be performed. Additionally, an appreciation of the variation possible in endocrine responses among the species to be studied must be obtained.

No abstract