LC50/LD50
LC50: (Lethal Concentration) is the concentration of the chemical in the air or water that will kill 50% of the test animals
LD50: (“Lethal Dose”) is the amount of a material, given all at once (injected/oral), which causes the death of 50% (one half) of a group of test animals, is one way to measure the short-term poisoning potential (acute toxicity) of a material.
Biotic Stress
is stress caused by living organisms
- predation, competition, population density, food shortage, pathogens and parasitism
abiotic is by non living things like sunlight, temperature etc
Biotic stressors can affect the chemicals’ bioavailability and toxicokinetics. They can also influence the behavior and physiology of organisms, which could result in an increased uptake and sensitivity to chemicals.
For Ceriodaphnia dubia, Qin et al. (2011) demonstrated that predator stress influenced the toxic effects of several pesticides differently. While predator cues interacted antagonistically with bifenthrin and thiacloprid, they acted synergistically with fipronil
Multistress
a situation in which an organism is exposed both to a toxicant and stressful environmental conditions.
Endpoints
The response of the test organisms is determined by monitoring selected endpoints, like survival, growth, reproduction or other parameters. Endpoints can increase (e.g. mortality) or decrease with increasing exposure concentration (e.g. survival, reproduction, growth).
Non conventional are endpoints that are not standardized in the oecd (OECD is for test guidelines)
concentration-response curves
visually maps how a biological system’s response changes as the concentration (or dose) of a chemical (like a drug or toxin) varies, typically showing a sigmoidal shape where increasing concentrations lead to a greater effect, plateauing at a maximum response (Emax), and revealing key metrics like EC50 (concentration for 50% effect) to assess potency and efficacy
Characterized by four parameters:
1. The minimum response is often set to the control level or to zero.
2. The maximum response is often set to 100%, in relation to the control or the biologically plausible maximum (e.g. 100% survival)
3. The slope identifies the steepness of the curve, and determines the distance between the EC50 and EC10.
4. The position parameter indicates where on the x-axis the curve is placed. The position may equal the EC50 and in that case it is named the turning point.
Toxicity calculations
ECx / EDx:
ECx = effective concentration causing an x% effect;
EDx = effective dose causing an x% effect (relative to control, endpoint specified).
LCx / LDx:
LCx: lethal concentration causing death in x% of organisms
LDx: lethal dose causing death in x% of organisms
* Both refer specifically to lethality as the endpoint.
EC50 / ED50:
EC50: the concentration that causes 50% of the maximum effect compared to the control
ED50: the dose that causes 50% of the maximum effect
* They are the most commonly used toxicity measures and must always be reported together with the specific endpoint (e.g. growth inhibition, reproduction).
LC50 / LD50:
LC50: concentration that causes death in 50% of exposed organisms
LD50: dose that causes death in 50% of exposed organisms
* Both refer specifically to lethality as the endpoint.
this is about notation, not a different concept:
LDx is the general term
Used when x can be any percentage (e.g. LD10, LD25, LD50)
LD50 is a specific case of LDx
Used when the effect level is exactly 50% lethality
So:
Use LDx when you want to stay general or when x ≠ 50
Use LD50 when you specifically mean median lethal dose
Difference meaning of dose and concentration in toxicity calculations
Concentration describes exposure in the environment, while dose describes what the organism actually receives.
There are also computerized values that can be calculated using this curve
Where the ECx are derived by curve fitting, the NOEC and LOEC are derived by a statistical test comparing the response at each test concentration with that of the controls.
Usually an Analysis of Variance (ANOVA) is used combined with a post-hoc test, e.g. Tukey, Bonferroni or Dunnett, to determine the NOEC and LOEC.
SSD (Species Sensitivity Distribution)
SSD is a distribution describing the variance in sensitivity of multiple species exposed to a hazardous compound. (SSD is built from multiple concentration-response results, containing multiple species to look at an ecosystem for example. )
- The statistical distribution is often plotted using a log-scaled concentration axis (X), and a cumulative probability axis (Y, varying from 0 – 1.
SSD you have the most sensitive species to that chemical on the left of the graph as they have an EC50 at the lowest concentration and the least sensitive species on the right as they are effected only at a higher concentration.
Step 1: Ecotoxicity data for creating a SSD model -> information is collected from published work on concentrations of substance on specific animals, so the ssd is based on ecotx data.
Step 2: The makeing and evaluation of an SSD model -> Standard statistical software (a spreadsheet program) or a software model (such as ETX) can be used to create a SSD from the found data.
Step 3a: The SSD model used for environmental protection -> to derive reference levels, like the PNEC, by using ecotoxicity data (NOECs or low-effect ECx values) from chronic tests to create an SSD-NOEC or SSD-ECx. A protective concentration, the HC5, is calculated so that 95% of species are expected to be unaffected, and this value often serves as the regulatory PNEC or Environmental Quality Standard (EQS).
Step 3b: The SSD model used for environmental quality assessment -> used to assess environmental damage by calculating the Potentially Affected Fraction (PAF) of species. PAF indicates the fraction of species likely affected (e.g., above their NOEC or EC50), allowing evaluation of whether concentrations exceed regulatory reference levels. Using SSDs for multiple sites produces PAF values, which can be used to rank sites by their potential ecological harm.
SSD uses NOECs, ECx, or other endpoints from multiple species
Plots the variation in sensitivity across species
Used to derive protective concentrations like HC5/PNEC
So: you first get NOEC/LOEC/ECx for each species, then these values feed into an SSD to assess ecosystem-level protection.
Shannon Wiener index
expresses biodiversity in general terms as the number of species in relation to the number of individuals per species.
The index is higher for communities with more species, but also higher when the abundance is more equally distributed over species. A low index implies a community with a few very dominant species. Environmental pollution tends to increase dominance, i.e. a few species are favoured and many become rare
Structural diversity & functional diversity
Structural diversity is based on taxonomically described and classified species
functional diversity is based on the processes they execute, e.g. related to feeding types or to specific decomposition processes like nitrification or enzyme processes
Some examples of abiotic stress - toxicitiy
Temperature:
Higher temperatures generally increase toxicity in cold-blooded organisms by increasing activity, uptake, and metabolic rate, while freezing temperatures can enhance toxicity through membrane damage.
Food:
Low food or nutrient availability increases toxicity because organisms have less energy for detoxification and repair. For example, daphnids exposed to thiacloprid under low-nutrient conditions were up to 2500× more sensitive than in laboratory tests, while high food availability reduced toxicity.
Salinity:
Salinity can either increase or decrease toxicity depending on the chemical and species. Metal toxicity often decreases with higher salinity due to ion competition, whereas some insecticides become more toxic.
pH:
pH affects both organism performance and chemical bioavailability. Outside optimal pH ranges, organisms are stressed, and for metals and ionizable chemicals, pH strongly alters speciation and uptake, changing toxicity.
Drought (soil):
Low moisture stresses soil organisms and can enhance chemical toxicity, especially for species dependent on moist conditions (e.g. earthworms, springtails), when chemicals impair membrane function or drought tolerance.
Why study ecotoxicology at community level?
Community ecotoxicology
study of toxicant effects on patterns of species abundance, diversity, community composition, and species interactions in a community.
Key phenomena: shifts in dominant species, loss or gain of species, altered predator–prey and competitive relationships, and changes in ecosystem processes.
Indirect effects in community ecotoxicology: arise when a toxicant affects one species, which then changes interactions and indirectly affects others (e.g. killing predators leads to temporary prey increase).
Interperating challanges: Interpretation focuses on separating toxicant‑driven changes from natural temporal development and variability among control cosms.
Challenges: complex indirect effects, huge datasets, differing trajectories during recovery, metapopulation influences, habitat heterogeneity, and strong dependence on timing and state of the community.
Communities are studied in mesocosms (controlled, semi‑natural experimental system for community/ecosystem studie), artificial ponds/ditches/streams, field set‑ups with in‑ or exclosures, or scaled‑down biofilm communities on small substrates.
Indoor multi-species tests are referred to as multicosms (lab based), whereas outdoor multi-species tests are called mesocosms (in the field).
Data are analyzed using multivariate methods (Multivariate analysis, statistics that analyze patterns in many species/variables simultaneously in community data., ecological indices (e.g. species richness) or effect classes, sometimes combined with species sensitivity distributions.