Stressor Dose Response Relationship

The relationship between the exposure dose to a stressor and the response from an entity receiving the stressor is described by stressor dose-response models. An example of such a model (curve) could be an ecological dose-response relationship expressed graphically from a retrospective approach whereby the ecological response is measured along a continuum of human disturbances already existing in a region. It could also be in form of measurements and quantification of levels of a chemical pollutant such as heavy metal contamination of soil or water and the corresponding response that can be measured enzyme activity in the medium under investigation. Different forms of dose-response models exist, but there are four generic models commonly used to describe them. Figures 4a-4d depict such kind of models. In these models, the magnitude of the stressor dose is plotted on the x-axis and the corresponding quantified response from the stressor is plotted on the y-axis as percentages and it is a measure of standard response. A stressor-response profile is usually the final product of a stressor-response analysis. It relates the magnitude of the effect to the magnitude, duration, frequency, and timing of exposure.

Figure 4a has a linear part and two threshold parts (one at a low magnitude of exposure and the other at a high magnitude of exposure). At the linear part, an increase in the magnitude of exposure brings about a decrease in response. This type of response is observed at the population level, for example, a decrease in prey items as the number of predators increases. An abrupt change in response with an increased magnitude of exposure is only observed where an increased in magnitude of exposure is slightly higher than the first threshold level. With the linear-part-type models, the stronger the exposure the steeper the linear part will be. Generally, at the threshold part of the curve, an increase in the magnitude of exposure has no effect on the response. At the second threshold level, an increase in exposure magnitude did not bring a change in response since the minimum response had already been achieved. Figure 4b has a practical threshold in the low levels of exposure which resulted in an increase in response. Figure 4 showed asymptotic rate of change of response. Here, at low magnitude of exposure, the change in response rate was so small to be considered negligible but as the exposure magnitude increases there is also steep change in response. Figure 4d has just the linear part of Figure 4a with no threshold levels.

More often, causal evaluation is used to identify factors that are responsible for observed effects such as the criteria developed by Hill in 1965 for establishing causality (Table 1).

The integration of stressor-response and exposure profiles include: (1) comparing single effects and exposure value; (2) comparing distribution of effects and exposure; and (3) conducting simulation modeling. The choice of any of these depends on the original purpose of the assessment as well as data available and time. A typical stressor-response curve is shown in Figure 5. This curve shows the ecological response on the j-axis and the stressor on the x-axis. Note that unlike in traditional dose-response curve, the units for either of the axes vary depending on the assessment being conducted. Allowance is usually made for a predetermined threshold that is considered acceptable as shown in the graph.

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Figure 4 Dose-response curves showing (a) an abrupt change in response with dose, (b) subsidy at low doses that can serve as a practical threshold, (c) asymptotic with a practical threshold, and (d) no threshold. Reproduced by permission of Taylor & Francis.

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Figure 4 Dose-response curves showing (a) an abrupt change in response with dose, (b) subsidy at low doses that can serve as a practical threshold, (c) asymptotic with a practical threshold, and (d) no threshold. Reproduced by permission of Taylor & Francis.

Table 1 Hill's criteria for evaluating causal associations

1. Strength of effect: A high magnitude of effect is associated with exposure to the stressor

2. Consistency of occurrence: The association is repeatedly observed under different circumstance

3. Specificity of effect to a stressor: The effect is diagnostic of a stressor

4. Temporality: The stressor precedes the effect in time

5. Presence of a biological gradient: A positive correlation between the stressor and response

6. Plausible mechanism of action

7. Coherence: The hypothesis does not conflict with knowledge of natural history and biology

8. Experimental evidence

9. Analogy: Similar stressors cause similar response

Source: US Environmental Protection Agency (1992) Framework for ecological risk assessment. EPA-Risk Assessment Forum, EPA/630/ R-92/001, Washington, DC.

Berettermodellen

According to the USEPA framework for ecological risk _

assessment, the stressor-response model may focus on Increasing rntenaty of stressor (dose)

different aspects of the stressor-response relationship Figures A typical sigmoidal curve for stressor-response depending on the objective of the assessment, the relationship (dose/percentage of mortality).

conceptual model, and the type of data used for analysis. Also crucial is the temporal and spatial distributions ofthe stressor in the experimental or observational setting. In the case of physical stressors, specific attributes of the environment after disturbance can be related to response.

Stressor (dose)-response relationships curves usually involve the derivation of indices of toxicity such as ecological dose (ED50), or EC50 similar to the lethal dose (LD50). Such descriptors convey useful information necessary for assessing the level of toxicity associated with the substance under investigation. These indices essentially describe the dose of the stressor or chemical necessary to produce 50% death or inhibition of the organism used for testing.

The LD50 is defined as the lethal dose at which 50% of the population is killed in a given period oftime; an LC50 is the lethal concentration required to kill 50% of the population. In ecological risk assessment, EC50 may be used instead of LD50; whereas LC50 is a measure of concentration (e.g., mgl—*), it could also be a specific temperature or any other parameter in a different unit of measure. These bioassays involve subjecting several replicate groups of individuals to a range of concentrations (or doses) of a toxic compound and measuring the mortality after a defined time interval that can range from minutes to hours or days. The data are then plotted and the lethal dose of interest interpolated from the graph as shown in Figure 5.

The curve shows a range of response to varying stressor intensity; the points are commonly used levels of effect estimating lethal dose (LD) fatal to a given percent of organisms in a population. More complex relationships typical of ecological risk assessments with multiple stressors and cumulative ecological effects may differ slightly and EC may be used in place of LD50. The final outcome of the stressor dose-response relationship feeds the final stage of risk assessment involving the characterization of the toxin in human risk assessment or the preparation of a stressor profile in ecological risk assessment. Note that on a large scale such as ecological risk assessment conducted for major ecosystems, the stressor dose-response models or curves will only provide a scientific framework for establishing how bioindicators (when present) respond to increasing human disturbance. Other factors such as the establishment of thresholds has to invoke sociopolitical factors; for example, society must set the threshold by considering tradeoff between economic growth and the level of ecological risk society may be willing to accept.

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