Response

The adverse ecological effects suffered as a result of exposure to stress is termed a 'response' (toxic reaction in toxicology). Reponses from an entity receiving a dose of a specific stressor could lead to changes in function or health of that entity receiving that stressor. Responses could be a reaction from either/both biotic and abiotic stressors.

Predation is a biotic stressor which has its response observed at a population (prey item) level. There are some similarities between response to a biological stressor and response to an abiotic stressor. For example, a disease could be a response to exposure to pathogenic bacteria or exposure to chemical pollutant. In both situations, the response could be observed at individual, population, community, and ecosystem level through the responses manifested at the molecular level of an individual. Responses could be detected at molecular, cellular, organ, organism, community, and ecosystem levels. An example of an entity responding at a molecular level from exposure to an abiotic stressor such as lead is the inhibition of aminolevulinic acid dehydratase (ALAD) in human and other organisms. This kind of response at a molecular level could be used as a biomarker of lead exposure and could serve as an early warning system for Pb contamination of an environmental medium. ALAD inhibition in organism is specific to lead exposure but other biomarkers are nonspecific. The nonspecific bio-markers indicate that harm is being caused but does not indicate which stressor is causing the harm. An example is the induction of monooxygenases. Monooxygenase enzyme is induced by a host of environmental chemicals including PCBs, DDT, dichlorodiphenyldichloroethy-lene (DDE), etc. Molecular-level responses could lead to response at cellular level, for example, cytotoxicity. Cytotoxicity can lead to the dysfunction of organs producing an organ-level response. An organ-level response can lead to response at the organism level. A typical example of organism-level response is decrease in reproduction; such a decrease in reproduction leads to a decline of the organism's population. Decrease in populations could lead to response observed at community level and finally community-level response could lead to responses observed at the ecosystem level.

Unlike the traditional dose-response in humans with definite assessed endpoint, for example, cancer resulting from exposure to environmental carcinogens, responses in ecological risk assessment vary considerably and can be a source of contention even when experimental evidence exists that links the stressor under consideration to the effects. The reason for this is not unconnected to the social and political/legal dimension that often comes to bear on ecological risk analyses, not the least of which are the variety of species, ecological communities, and ecological functions from which to choose, and the statutory ambiguity regarding what needs to be protected. Some known examples of ecological responses at the ecosystem levels include (1) 'forest decline' in Europe in the 1980s, resulting from a combination of stressors that included acid rain, elevated ozone levels, fogs, and frost following drought years; (2) the dwindling growth of maple seedlings attributed to acid rain as stressor in northeastern United States, inhibition of nitrogen-fixing ability of nitrogen-fixing bacteria species in the soil, and the consequent reduction in yields of legumes and (3) bird kill resulting from chemical spill, or from long-term bioconcentration of toxic chemicals or fish kill, resulting from the Exxon Valdez oil spill of the 1990s in Alaska. Regardless of these responses, however, it is important to establish true linkage between the environmental stressor and the endpoint. Recently, the US Environmental Protection Agency (USEPA) published a document that describes a set of endpoints known as generic ecological assessment endpoints (GEAEs) that can be considered and adapted to specific ecological risk assessments for improving the scientific basis for ecological risk-management decisions.

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