In real world scenarios, organisms are usually exposed to multiple environmental rather than individual stressors in the environment. Not only does this mixture of stressors differ qualitatively, they also differ in terms ofquantity. In addition, a stressor to an entity may also constitute a stressor to another entity in the same ecosystem, directly or indirectly. To understand the nature of responses emanating from complex mixtures of stressors, for example, one therefore needs a clear understanding about the functioning of that particular ecosystem and the mechanism of interaction among the interacting environmental stressors. In addition, one needs to know how biotic systems interact with each other as well as with these complex mixtures of stressors in the ambient environment. The interaction between an entity and specific quantity of stressor(s) produces stressor dose-response relationship (simply dose-response in human toxicology), which when appropriately quantified or modeled will provide pertinent information establishing the extent of stressors and the corresponding magnitude of adverse effects in risk assessment.
Stressor dose-response models are graphical representation of quantifiable stressors and responses depicting real causal relationships between the two variables, that is, dose and response, and used as an indispensable component of human or ecological risk assessment for guiding policy and risk-management decisions. Stressor dose-response relationship is one of the major steps in ecological risk-assessment processes. It depicts the change in response upon exposure to differing levels of stressor. Figure 3 describes processes involved in ecological risk assessment with particular reference to the stressor dose-response relationship as an integral part of the process; the others being exposure assessment, response assessment, and risk characterization. Response to a stressor depends on the quantity of the stressor and the type of biological organism receiving the stressor.
The assumptions on which the stressor dose-response relationships can be successfully based are (1) that the response is based on the knowledge that the response produced is actually due to known stressor/toxic agent(s), (2) that the response is in fact related to the dose of the stressor, and (3) that the stressor dose-response relationship is based on the existence of a quantifiable method of measuring and a precise means of expressing the effect of the stressor. When a large quantity of a specific stressor is used for a short time, the corresponding response is normally a complete destruction of the entity. This type of exposure is known as acute. For example, natural disasters like earthquake, tornadoes, hurricanes, volcanic eruption, tsunami, etc., could be considered as acute events because they occur for a very short time and the effect is usually catastrophic. Another example of acute events is fish kill in highly eutrophic waters during very hot summers. On the other hand, if a small quantity of stressor is applied for a very long time, the exposure is referred to as chronic. In chronic exposure, there is no lethality or destruction but a major functional physiology of the entity could be affected. For example, egg shell thinning in birds exposed to low levels of DDE for a long period of time caused the bird's population to decline. On a global scale, the gradual increase in carbon dioxide concentration could be considered a chronic event and the plausible response is global warming. Global warming has been linked to sea-level rise resulting from polar ice melting; hence the response from the global ecosystem as the result of gradual increase in carbon dioxide concentration is the rise in sea level.
The LC50 is one way to measure the short-term potential effect of a stressor at a very high quantity. It refers to a concentration of a stressor in an ambient environment which kills 50% of a sample population. Although many
endpoints are quantitative and precise in human risk assessment, they are often indirect measures of toxicity. For example, changes in enzyme levels in blood can indicate tissue damage. Many direct measures of effects are not necessarily related to the mechanism by which a stressor produces its harm to an entity but have the advantage of permitting a causal relationship to be established between the agent and its action. For new chemicals, however, it is customary to use lethality as a starting point or index of toxicological evaluation.
Response from an abiotic component of an ecosystem could be a decrease in the suitability as a habitat for resident organisms. Since organisms obtain benefits such as ecosystem services including but not limited to food and waste assimilation from a properly functioning ecosystem, a decrease in suitability of such a habitat could jeopardize the existence of the organism. Another example of response from abiotic stressor is changes in land use such as a rural community becoming urbanized. This type of change in land use could adversely impact both the terrestrial and aquatic coastal ecology, particularly where intensive crop and animal husbandry are replaced by industry and real estate. Once there is a change in land use, the response associated with the new land use could be different depending on the nature of the new stressor.
For example, cultural eutrophication is a major problem associated with most coastal zones due to disposal of household waste into these zones. The stressor in this situation is increase in nutrients from human wastes living in the area. The response from such activity will be oxygen depletion resulting in fish kill. Fish kill has negative impact on fish populations but this same stressor could produce a different response on other organisms such as phytoplankton bloom in this coastal zone where eutrophication is taking place. For example, opportunistic plant species dwelling in such eutrophic waters will respond positively to this stressor by blooming. Central to defining levels of exposure deemed safe or unsafe for environmental stressors is studying exposure-response and developing exposure-response models needed for ecological risk assessment for public policymakers.
Was this article helpful?