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The last half-century has shown a dramatic increase in the standard of living of millions of people in Europe, North America and many parts of the Third World. This has, in many ways been brought about by scientific and technical developments which were initiated in the 1940s and 1950s. Promises were then made that nuclear energy would provide electricity so cheap that it would not need metering, pesticides would end malnutrition throughout the world and plastics and other synthetic chemicals would revolutionise our manufacturing industry and our way of life. Whilst some of these promises have been fulfilled, the problems of long-term health risks to humans and wildlife arising from the use, production and disposal of these products were either unknown or deliberately understated. Nuclear power is rendered economically unviable when the real cost of decommissioning and storage of waste for several millenia is included, and the effects on health of both humans and wildlife of early pest eradication programmes with organochlorine pesticides were well documented in Rachel Carson's "Silent Spring". Evidence of the effects of aerosols and refrigerants on depletion of the ozone layer has led to restriction on the use of CFCs, and there is now increasing evidence of climate change resulting from our profligate use of fossil fuels.
The applicability of male plasma vitellogenin as an indicator of reproductive dysfunction in estrogen-treated cunner was investigated. Results suggest that male plasma vitellogenin is not a reliable indicator of reproductive impairment.
Environmental pollutants are suspected of causing observed adverse effects on development and reproduction in fish and wildlife. Evidence from the laboratory and field suggests that low levels of synthetic or natural chemicals that modulate or disrupt endocrine processes may be responsible. The aquatic environment is a sink for most all potential endocrine disrupting chemicals (EDCs). From egg fertilization to spawning, fish may be exposed to complex mixtures of steroidogenic chemicals that can interfere with the important activational and organizational processes of their endogenous hormones. One consequence of exposure to EDCs may be disruption of the normal mechanisms of sexual development and differentiation, processes that are highly hormone dependent, with subsequent adverse effects on reproduction. My experiments address the hypothesis that exposure to EDCs during early ontogeny affects sexual development and differentiation in fish manifest at maturation. The dr-R strain of medaka was used as the test organism because of qualities that make it a good laboratory animal model and because it possesses a sex-linked gene for body color allowing visual determination of genetic sex from hatch. Medaka were exposed in ovo by nano-injection to five chemical compounds known or suspected to be hormone mimics or disruptors. Details of the effects resulting from exposure to the synthetic sex steroids ethinyl estradiol (EE 2) and methyl testosterone (MT) provided a reference and established a model for predicting effects of in ovo exposure to chemicals which mimic estrogens and androgens. Effects on medaka exposed to the EDCs, o, p ' -DDE and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and three mixtures of polychlorinated naphthalenes (PCN), which have not been tested for their endocrine disrupting potential, were also investigated. In ovo exposure to 0.5 and 2.5 ng EE 2 /embryo or 0.8 and 8.0 ng MT/embryo affected sexual differentiation by causing sex reversal in males and females, respectively. Sexual development of male and female gonads was also affected at these doses. Most notably, all doses of MT resulted in precocious maturation of male and female medaka. Effects on sexual differentiation of the gonads were not as apparent for o, p ' -DDE, TCDD, and the PCNs as were effects on sexual development. Observed effects of these chemicals included one or more abnormalities: histopathological lesions (e.g., atresia), reduced gonad size, and changes in primary germ cell numbers along with volume of primordial gonads. Results for these chemicals together with other's field and laboratory observations provide further evidence that environmental EDCs may be adversely affecting reproduction and development of wild fishes. These results also support the utility of laboratory studies with the dr-R medaka model within the framework of a weight-of-evidence approach to establish a cause-and-effect relationship between environmental exposure to EDCs and reproductive impairment at the individual and population levels.
Some investigators have hypothesized that estrogens and other hormonally active agents found in the environment might be involved in breast cancer increases and sperm count declines in humans as well as deformities and reproductive problems seen in wildlife. This book looks in detail at the science behind the ominous prospect of "estrogen mimics" threatening health and well-being, from the level of ecosystems and populations to individual people and animals. The committee identifies research needs and offers specific recommendations to decision-makers. This authoritative volume: Critically evaluates the literature on hormonally active agents in the environment and identifies known and suspected toxicologic mechanisms and effects of fish, wildlife, and humans. Examines whether and how exposure to hormonally active agents occursâ€"in diet, in pharmaceuticals, from industrial releases into the environmentâ€"and why the debate centers on estrogens. Identifies significant uncertainties, limitations of knowledge, and weaknesses in the scientific literature. The book presents a wealth of information and investigates a wide range of examples across the spectrum of life that might be related to these agents.