Wildlife exposures reproductive toxicants

Much of the evidence for the adverse reproductive effects of selected toxicants will be based on cases involving wildlife exposures to environmental contaminants or on the experimental results of research exposing laboratory animals to large, pharmacological doses of potential toxicants. When available, data will be presented from accidental or intentional human and domestic animal exposures to toxicants associated with riot control and chemical warfare or with environmental catastrophes where incidences of infertility, abortion, and teratogenesis have been traced over the course of a number of years. 

Based on the observations of reproductive toxicity (including endocrine disruption) in wildlife and domestic animals, as well as ongoing concerns about reproductive dysgenesis in human populations and the observed effects of industrial accidents involving MIC and dioxins, there has been increasing interest in the effects of prenatal exposures of humans to suspected endocrine disrupters and other reproductive toxicants. However, when impaired reproductive function is discovered in adults, it is difficult to comment with complete certainty on the relative contributions of prenatal versus postnatal exposures to reproductive toxicants. There is a wide array of pesticides and other organic environmental... 

Data for PCP and terrestrial wildlife are incomplete and — in view of the large interspecies variations in sensitivity — need to be collected. Research is needed on reproductive effects in animals following inhalation exposure to PCP additional acute and intermediate toxicity testing chronic duration exposure studies on cancer induction, genotoxicity, and immunotoxicity and the development of alternate biomarkers of PCP exposure and antidotes (WHO 1987 USPHS 1994). Until the results of these studies become available, it seems reasonable to apply to wildlife the same levels recommended for human health protection. 

In the Green Screen the hazards of a chemical are defined by its potential to cause acute or chronic adverse effects in humans or wildlife, its fate in the environment, and certain physi-cal/chemical properties of concern to human health. Acute mammalian toxicity (lethality) and irritation of the skin or eye are examples of acute adverse effects that can result from inhalation, ingestion, or dermal contact with a chemical. Chronic effects occur after repeated exposures and include cancer and adverse effects to the reproductive, neurological, endocrine, or immune systems. 

The effect of these compounds on human health has been a major cause of concern. Toxicity to humans depends on exact structure, but exposure is ubiquitous and involves a mixture of compounds, from fossil fuel and natural and anthropogenic burning and from food, mainly grilled or barbecued meat. In the broader environment, PAHs are endocrine disruptors and bind to the aryl hydrocarbon receptor. They have been shown to depress immune function in some wildlife. They may be responsible for reproductive disorders in aquatic organisms, especially in shellfish and sediment dwellers. 

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