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Pollution-induced community tolerance

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Pollution-Induced Community Tolerance (PICT) is an approach to measuring the response of pollution–induced selective pressures on a community. It is an eco-toxicological tool that approaches community tolerance to pollution from a holistic stand point. Community Tolerance can increase in one of three ways: physical adaptations or phenotypic plasticity, selection of favorable genotypes, and the replacement of sensitive species by tolerant species in a community.

PICT differs from the Population Tolerance Approach to Community Tolerance in that it can be easily applied to any ecosystem and it is not critical to use a representative test organism, as with the Population Tolerance Approach.

Community Tolerance

Community tolerance can be used as indicator for determining if a toxicant has a disturbance on an exposed community for multiple types of organisms.[1] Tolerance of a toxicant can increase by three ways; physiological adaptation also known as the phenotypic plasticity of an individual, tolerant genotypes selected within a population over time, and the replacement of species with more tolerant ones within a community.[2] Physiological adaptation, or phenotypic plasticity, is the ability of an individual organism to change its phenotype in response to changes in the environment.[3] This can occur with huge variance between the type of organism and the type of the disturbance they experience. Natural selection that occurs over several generations causes an entire population to exhibit specific selection of genotypes.[4] Overtime, tolerant genotypes can be selected over non tolerant ones and can cause a shift in a population’s genome.[5] Natural selection can also cause a replacement of less tolerant species with more tolerant species.[4] All of these aspects can alter a communities’ structure drastically and if a toxicant can be identified as the culprit, action can take place to prevent that toxicant from further accumulating .[1] PICT can be used for linkage between cause and effect of the toxicants due to the structure of a community that has survived the event also known as toxicant-induced succession (TIS).[5] Toxicant-Induced succession would be the development of more tolerant generations once a chemical was introduced into the environment.

There are two types of tolerances that can occur; multiple and co-tolerance. Multiple tolerances can elevate an individual’s ability to tolerate several toxicants present at once.[2] This means that depending on the type of chemicals present in the environment, the concentration, and the organisms that are affected could alter the environment in multiple different ways. Co tolerance is the ability of an organism to develop a tolerance to a certain toxicant in short term tests, and obtain that tolerance for other toxicants similar to the first.[2] Toxicant can cause co-tolerance for species if they’re closely related chemistry or have similar modes of action.[1] It can be difficult to determine with type of tolerance is occurring if there are multiple types of toxicants in a community because they could be acting simultaneously. Basically it is difficult to understand what exactly may be going on in a community without testing it with multiple ecotoxicological tools with long and short term toxicity tests.

Field Studies

Assessing Pollution Induced Community Tolerance can be done utilizing in situ techniques. Many of these techniques involve the use of known or created chemical exposure gradients. One such example is the use of a known concentration gradient of Tri-n-butylin to assess PICT in periphyton.[6] Tolerance patterns showed that tolerance was highest closest to the marina that was the source of contamination. The use of reference sites in addition to contaminated sites is also commonly used for translocation assessments of PICT. A study in Germany cultured periphyton on glass discs in two river systems north of Leipzig, Germany. One system was the contaminated area of study and the other was 10 km upstream and uncontaminated, intended to be used as a reference. After the colonization period, 6 of the 10 racks of glass discs were trans-located to the other river system. During the experiment the community structure present on the glass discs from the reference site, when translocated to the contaminated site changed to mirror that of the control discs that were left in the contaminated sites.[1] In another study in Denmark enclosure experiments were done allowing for an assessment of PICT utilizing the lake water from Lake Bure as a baseline. By using this water from the lake potentially confounding variables would be nullified by comparing results to the control. Concentrations of Atrazine and Copper were added to these enclosures in varying concentrations. As in other experiments previously discussed periphyton communities were used in this experiment and were cultured using glass discs. Photosynthetic activity was measured and used as a measurement of PICT throughout the experiment. The experiment showed that elevated levels of Cu lead to community tolerance of the phytoplankton community as well as co-tolerance of zinc. Total Biomass decreased at the outset of the trials involving high concentrations of Cu indicating that Community Tolerance was increased due to direct mortality of the sensitive species.[7]

The use of PICT in an in situ fashion is not limited to aquatic systems. A study involving 2,4,6-Trinitrotoluene utilized respirometric techniques to measure Pollution-Induced Community Tolerance in soil microbial communities in response to the presence of TNT. The results of this study further corroborate the PICT Theory, in that treatments with long-term exposure to TNT had a larger proportion of TNT-resistant bacteria than soils with low levels of TNT.[8] This PICT caused by TNT was also present in another study.[9]

Ideally Pollution-Induced Community Tolerance can be assessed in the field by using a representative sample of the natural community in response to environmental contamination, however this is not always the case which is why the use of laboratory studies are necessary supplements to properly assess PICT.

Lab Studies

The laboratory investigation of PICT is necessary to eliminate factors other than pollution that may affect community structure.[2] It can be conducted in conjunction with field work, as in the study by Blanck and Dahl (1996). In this study, the results from laboratory acute toxicity tests of TBT on periphyton corroborated the results from the field study, supporting the conclusion that toxicity to periphyton resulted from TBT pollution at the site under investigation.[6] The results from acute toxicity tests can thus help determine whether the effect identified is due to a specific contaminant.

There are a variety of methods for laboratory testing, but a general format includes sampling, a bioassay, and an analysis of community structure.

Samples can be collected on artificial or natural substrata, either in situ or in the laboratory.[10] There must be a series of samples exposed to different concentrations of contaminant and a control sample. In situ sampling involves setting up a sampling device in an aquatic ecosystem and allowing it to colonize for some time (e.g. a couple of weeks). One example is the diatometer, a device that is deployed in the water that becomes colonized by diatoms, and then is removed for analysis.[11] In situ sampling devices are set up at increasing distances from the pollution source in the case of point source pollution. The samples thus represent a gradient in contaminant concentration, assuming that the contaminant becomes more dilute with increasing distance from the point source. An example of laboratory sampling was used in a study by Schmitt-Jansen and Altenburger (2005). For 14 days communities were allowed to establish on discs set up in laboratory aquariums which were continuously mixed and inoculated with algae from a pond. The aquariums were dosed with different concentrations of herbicide to get a gradient of long-term (14-day) contaminant exposures. Once a week the aquarium water was completely replaced and re-dosed with herbicide.[12]

A bioassay is conducted on the samples to test for correlation between tolerance and long-term contaminant exposure. First, samples are exposed to different concentrations of contaminant. Then an endpoint is measured to determine the toxic effect on the sample organisms. The results from these measurements are used to produce an EC50.[12] Both Blanck (1996) and Schmitt-Jansen and Altenburger (2005) photosynthesis as their endpoint.[6][12]

Community structure of the samples is analyzed to check for a correlation between species prevalence and long-term contaminant exposure. Samples are taxonomically classified to determine the composition and species diversity of the communities that established over the long term exposures. The results are compared to the concentration of contaminant in the long-term exposure to conclude if a relationship was found in the study.[12]

References

  1. ^ a b c d Rotter, Stefanie; Sans-Piche, Frederic; Streck, Georg; Altenburger, Rolf; Schmitt-Jansen, Mechthild (2011). "Active Bio-monitoring of Contamination in Aquatic Systems—An in Situ Translocation Experiment Applying the PICT Concept". Aquatic Toxicology. 101 (1): 228–236. doi:10.1016/j.aquatox.2010.10.001.
  2. ^ a b c d Blanck, Hans; Wangberg, S. A.; Molander, S. (1988). "Pollution-Induced Community Tolerance - A New Ecotoxicological Tool." Functional Testing of Aquatic Biota for Estimating Hazards of Chemicals". American Society for Testing and Materials. STP. 988: 219–230.
  3. ^ Miner, Benjamin G., Sonia E. Sultan, Steven G. Morgan, Dianna K. Padilla, and Rick A. Relyea. 12 December 2005. "Ecological Consequences of Phenotypic Plasticity." Elsevier. Trends in Ecology and Evolution. 20 (12): 685-692). http://bama.ua.edu/~rlearley/Miner_2005.pdf.
  4. ^ a b Darwin, Charles. 1859. "Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life." London: John Murray. 1st Edition. http://graphics8.nytimes.com/packages/images/nytint/docs/charles-darwin-on-the-origin-of-species/original.pdf
  5. ^ a b Blanck, Hans. 22 September 2010. “A Critical Review of Procedures and Approaches Used for Assessing Pollution-Induced Community Tolerance (PICT) in Biotic Communities, Human and Ecological Risk Assessment.” Human and Ecological Risk Assessment: An International Journal. 8 (5): 1003-1034. http://www.tandfonline.com/doi/pdf/10.1080/1080-700291905792.
  6. ^ a b c Blanck, Hans; Dahl, Bjorn (1996). "Pollution-induced Community Tolerance (PICT) in Marineperiphyton in Agradient of Tri-n-butyltin (TBT) Contamination". Aquatic Toxicology. 35 (1): 59–77. doi:10.1016/0166-445X(96)00007-0.
  7. ^ Gustavson, Kim; Wangberg, Sten-Ake (1995). "Toleranceinduction and Succession in Microalgae Communities Exposed to Copper and Atrazine". Aquatic Toxicology. 32 (4): 283–302. doi:10.1016/0166-445X(95)00002-L.
  8. ^ Gong, Ping; Gasparrini, Pietro; Rho, Denis; Hawari, Jalal; Thiboutot, Sonia; Ampleman, Guy; Sunahara, Geofrrey I. (2000). "An in Situ Respirometric Technique to Measure Pollution-Induced Microbial Community Tolerance in Soils Contaminated with 2,4,6-Trinitrotoluene". Ecotoxicology and Environmental Safety. 47: 96–103. doi:10.1006/eesa.2000.1934.
  9. ^ Siciliano, Steven D.; Gong, Ping; Sunahara, Geoffrey I.; Greer, Charles W. (2000). "Assessment of 2,4,6-Trinitrotoluene Toxicity in Field Soils by Pollution-Induced Community Tolerance, Denaturing Gradient Gel Electrophoresis, and Seed Germination Assay". Environmental Toxicology and Chemistry. 19 (8): 2154–160. doi:10.1002/etc.5620190827.
  10. ^ Blanck, Hans. 1985. “A simple, community level, ecotoxicological test system using samples of periphyton”. Hydrobiologia. 124: 251-261.
  11. ^ “Tools of a Scientist”. Urban Rivers Awareness. 2004.
  12. ^ a b c d Schmitt-Jansen, M.; Altenburger, R. (2005). "Predicting and observing responses of algal communities to photosystem II-herbicide exposure using pollution-induced community tolerance and species-sensitivity distributions". Environmental Toxicology and Chemistry. 24: 304–312. doi:10.1897/03-647.1.