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Ecotoxicology Definitions

Some of the terms used in ecotoxicology, such as LD50, have simple, widely accepted definitions and hence can be defined here with some confidence. Others however vary quite widely in their interpretation from one text to another. I have tried to indicate these below and can only suggest that the reader refer carefully to the introduction of the text they are using. Where there is likely to be some contradiction I have listed the reference for the definitions given. Please add to this list by sending your definitions to me at


  • is concerned wit the toxic effects of chemical and physical agents on living organisms, especially on populations and communities within defined ecosystems: it includes the transfer pathways of those agents and their interactions with the environment. Butler, 1978.

  • investigates the effects of substances on organisms. The hazard to animal and plant populations can be determined by using survey data (retrospective) or by performing specific tests (prospective). Rudolph & Boje, 1986.

  • the science that seeks to predict the impacts of chemicals on ecosystems. Levin et al 1989.

  • the study of harmful effects of chemicals upon ecosystems. Walker et al 1996.


Depending on the source, environmental chemical may be used to describe simply a chemical that occurs in the environment (Walker et al 1996) or substances which enter the environment as a result of human activity or occur in higher concentrations than they would in nature (Römbke & Moltmann 1995).

The terms contaminant and pollutant can be described separately but are often in effect synonomous. Both are used to describe chemicals that are found at levels judged to be above those that would normally be expected. Pollutants have the potential to cause harm, whereas contaminants are not harmful. This is however, not an easy distinction to make. Whether or not a contaminant is a pollutant may depend on its level in the environment and the organism or system being considered, thus one particular substance may be a contaminant relative to one species but pollutant relative to another. Finally, in practice it is often difficult to demonstrate that harm is not being caused so that in effect pollutant and contaminant become synonomous. (Walker et al 1996).

Xenobiotic is used to describe compounds that are 'foreign' to a particular organism, that is they do not play a part in their normal biochemistry. A chemical that is normal to one organism may be foreign to another and so xenobiotics may be naturally occurring as well an man-made compounds (Walker et al 1996). Xenobiotic is sometimes also used in a more general sense to decribe "foreign substances" in the environment (Römbke & Moltmann 1995).


There is a fundamental difference is viewpoint beteen these two definitions, one defines harm as an effect regardless of any compensation that the population might make, the other defines damage as occurring only if there is an effect subsequent to any compensation.

harm: biochemical or physical changes which adversely affect individual organisms' birth, growth or mortality rates. Such changes would necessarily produce population declines were it not that other processes may compensate. (Walker et al 1996).
damage: "the interaction between a substance and a biological ssytem. The substance's potential to cause damage is weighed against the protective potential inherent in the biological system (e.g. excretion or metabolic reactions, adaptation or regeneration)" (Römbke & Moltmann 1995).


There are many different ways in which toxicity can be measured but they are nearly all assessed relative to a particular outcome or END POINT. Initially, most Toxicity Tests measured the number of organisms killed by a particular DOSE or CONCENTRATION of the chemical being tested. With terrestrial animals the DOSE of chemical (taken orally, applied to the skin or injected) administered is usually recorded. DOSE is usually used where the dietry dose of a test chemical can be accurately determined. For aquatic organisms or where the test chemical is dosed ont the surrounding medium, the tests usually measure the CONCENTRATION of chemical in the surrounding water/medium.

The following measures, known as a group as EDs or ECs (Effective Doses or Effective Concentrations) are frequently used to describe data from toxicity tests:

Median lethal dose, that is the dose that kills 50% of the population
Median lethal concentration.
Median effect dose/concentration, that is the dose that produced a defined effect to 50% of the population.
No Observed Effect Dose (or Concentration)
No Observed Effect Level. Sometimes this more general term is used to describe either of the above. It can be defined as the highest level (that is dose or concentration) of the test chemical that does not cause a statistically signficant difference from the control.
Lowest Observed Effect Dose (or Concentration)

There has been a move away from the use of lethal end points in toxicity testing towards the measurement of EFFECTS rather than death. Examples of EFFECTS which can be used include changes in: reproduction (eg. number of eggs laid or young hatched); growth (e.g. biomass or body length) and biochemical or physiological effects (e.g. enzyme synthesis or respiration).


Toxicity data is used to make assessments of the HAZARD and the RISK posed by a particular chemical. Where:

the potential to cause harm
the probability that harm will be caused.

Defining HAZARD involves answering two questions, 'how much damage are we prepared to tolerate' and 'how much proof is enough'. The first is a question for society, alleviating/avoiding/repairing damage involves costs, how much are we prepared to pay? The second is largely a scientific problem of providing sufficient evidence that damage is due to pollution. HAZARD is not necessarily directly related to toxicity, it is a product of exposure and toxicity, a compound with moderate toxicity but very high exposure may cause more damage that a very toxic chemical with very low exposure.

RISK if usually defined using the predicted environmental concentration (PEC) and the predicted environmental no effect concentration (PNEC). Information on the movement and behaviour of pollutants in the environment are used to calculate the PEC whereas data from Toxicity Testing must be extrapolated to calculate the PNEC. The making of these calculations is not a precise art, apart from doubts about the extrapolation of Toxicity data from the lab to the field it can be very difficult to estimate the degree of exposure, particularly for mobile species such as birds and mammals.


A Biomarker can be defined as a "biological response to a chemical or chemicals that gives a measure of exposure and sometimes, also, of toxic effect" (Walker et al 1996), they can be divided into biomarkers of exposure and of toxic effect. Examples of biomarkers range from the inhibition of AChE (acetylcholinesterase) in the nervous system of animals to the thinning of eggshells in birds. Biomarkers can help to bridge the gap between the laboratory and the field by giving direct evidence of whether or not a particular animal, plant or ecosystem is being affected by pollution. They will often provide more reliable evidence of exposure than measurements of the pollutants themselves in the environment, the latter are often short-lived and difficult to detect, whereas their effects (detectable via biomarkers) may be much longer-term.


The difficulty in extrapolating from simple, highly artificial, single-species toxicity tests to complex, multi-variate ecosystems has led to attempts to develop more complex systems which can be used in toxicity tests. Such systems are usually termed microcosms, mesocosms or macrocosms, that is small, medium or large multispecies systems. It must be possible to control conditions in these systems to such an extent that they can provide meaningful, reproducable (that is, the system could be accurately copied elsewhere), replicable (that is, two replicates of the same experiment would produce the same results) data in toxicity tests. Simply because they are more complex systems it is seldom possible to produce tests that are as precise and controlled as those carried out in single species STTs. However, despite their limitations these larger-scale tests can provide important insights into the effect of pollutants on whole systems rather than on single species.


In natural systems, organisms are often exposed to more than one pollutant at the same time. Regulatory authorities usually assume - unless there is evidence to the contrary - that the toxicity of combinations of chemicals is roughly additive, and in many cases this is quite correct. However, in some cases, toxicity is more than additive that is there is POTENTIATION of toxicity. One particular type of potentiation called SYNERGISM occurs where only one of the chemicals present would cause a toxic effect on its own, when a particular second chemical is present it is not toxic in its own right but acts as a SYNERGIST to greatly increase the toxicity of the first chemical.