A proper review of reproductive toxicity within an eco-toxicological context should draw out a distinction between concerns over large geographical expanses and those that pertain to discrete and relatively small area locations. Examples of the former would be the US's Gulf States region, or the Eastern deciduous forest; an example of the latter would be a 5 ac hazardous waste
Reproduction See Mating Systems site that is managed under a program such as the US Environmental Protection Agency's (EPA) Superfund Program. For the large expanses, the chemical or chemicals responsible for reproductive effects typically have numerous release points, and have had wide-area distribution of the toxicants achieved by dynamic global processes, such as aerial transfer via wind entrainment. The very real problem of eggshell thinning in numerous bird species that came to our attention in the 1960s and 1970s, and that led to severe bird population declines, exemplifies this pattern. The extensive use of chlorinated organic pesticides for two decades prior, led to substantial accumulations of DDT and its associated metabolites in soil, which were conveyed to lakes and streams through overland flow events. Through bioaccumulation, the pesticides entered the birds' aquatic diet items, and interfered with shell deposition during development. This situation led to incubating eggs having their shells crack under the weight of nesting parents. Reproductive toxicity in this scenario entered the picture when it became apparent that eggshells were breaking during development, and when population declines were being noted. Thus, there was a critical need to assign toxicological causation to the discovered effects, and for a variety of reasons. First, with the reproductive toxin identified, man could intervene and ensure that further releases of the offending agents could be curbed. Second, toxicological principles could possibly be applied to minimize further impacts from the already-released organochloride pesticides. Finally, protocols could be developed to test other pesticides for their potential to induce reproductive effects prior to their commercial availability and use.
Within a context of discrete and relatively small contaminated properties (such as hazardous waste sites), the role of reproductive toxicity is entirely different. What triggers the development and application of such science is rarely the discovery of a population-impacting reproductive effect, but rather the anticipation that there could be one. The addition of the Superfund Program to the EPA's mission in 1980 required health risk assessments to be conducted for ecological receptors as well as for humans. The outcomes of the largely reproduction-based ecological assessments intend to either express an acceptable or unacceptable risk. In the latter case, the recommendation is made to study the issue further or to remediate the site outright, because it is assumed that continued chemical exposures will eventually trigger population-leveling effects. It is chiefly the ecological risk assessment (ERA) process of the Superfund Program and other similarly aligned initiatives that has fueled the interest in reproductive toxicity for ecological (i.e., nonhuman) species, and the generation of toxicological data over the last two decades or more to support such concerns.
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