Ecological death

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Ecological death is the inability of an organism to function in an ecological context, leading to death. [1] This term can be used in many fields of biology to describe any species. In the context of aquatic toxicology, a toxic chemical, or toxicant, directly affects an aquatic organism but does not immediately kill it; instead it impairs an organism's normal ecological functions which then lead to death or lack of offspring. The toxicant makes the organism unable to function ecologically in some way, even though it does not suffer obviously from the toxicant. Ecological death may be caused by sublethal toxicological effects that can be behavioral, physiological, biochemical, or histological. [2]

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Types of sublethal effects causing ecological death

Sublethal effects consist of any effects of an organism caused by a toxicant that do not include death. These effects are generally not observed well in a shorter acute toxicity test. [2] A longer, chronic toxicity test will allow enough time for these effects to appear in an organism and for them to lead to ecological death. [2]

Behavioral effects

Toxicants can affect an organism's behavior, which with aquatic organisms, may impact their ability to swim, feed or avoid predators. [2] The impacted behavior can lead to an organism's death because it may starve or get eaten by predators. [2] Toxicants may affect behavior by impacting the sensory systems which organisms depend on to collect information about their environment or by impacting an organism's motivation to properly respond to sensory cues. [1] If an organism is unable to use sensory cues effectively, they may be unable to respond to early warning signs of predation risk. [1] Toxicants can also affect later stages of predation by impacting an organism's ability to respond to predators or follow through with escape strategies. [1]

Physiological effects

Toxicants can affect an organism's physiology which may impact its growth, reproduction, and/or development. [2] If an organism does not grow correctly and is undersize or has growth defects, it will be more likely to be eaten by predators. If an organism's reproduction is impaired, it may not directly die, but it will be unable to pass on its genes to the population. The organism will no longer be representative in the population's gene pool.

Biochemical effects

Toxicants can alter the enzymes or ions present in an organism. [2] If this alteration does not directly cause death, but impacts the behavior or physiology of the organism, it can also lead to ecological death.

Histological effects

Toxicants can alter an organism's tissues. [2] If this alteration does not directly cause death, but impacts the behavior or physiology of the organism, it can also lead to ecological death.

Toxicant examples leading to ecological death

DDT

An effect caused by DDT is shell thinning in bird eggs, leading to the death of the chick. Once DDT has been accumulated by an adult bird, it is metabolized into the form DDE which is both stable and toxic. [3] Once in the form of DDE, the chemical impacts the metabolism of calcium in adult female birds’ shell glands, ultimately causing a decrease in eggshell thickness. [3] At high concentrations of DDT, the eggshells will no longer be able to support the incubating parents’ weight and will lead to the death of the unborn chick. [3] This is an example of physiological and biochemical sublethal effects leading to ecological death of the chick.

Diazinon

An effect caused by diazinon is a decrease in response to predator cues in Chinook salmon (Oncorhynchus tshawytscha). Diazinon, an organopesticide, was exposed to juvenile Chinook salmon for two hours at 1 and 10 μg/L, and these concentrations were enough to eliminate the behavioral responses of the fish to predator chemical cues. [4] If the fish cannot recognize that a predator is nearby, it is likely to be eaten. This is an example of a behavioral sublethal effect leading to ecological death.

Pentachlorophenol

An effect caused by pentachlorophenol is a decrease in response to predator attacks in guppies (Poecilia reticula). Pentachlorophenol was exposed to juvenile guppies at 500 and 700 μg/L, and both concentrations decreased the guppies’ reactions to predators. [5] The predators did not have to strike as frequently, did not have to pursue as frequently, or have to pursue the guppies as long as guppies that had not been exposed to these levels of pentachlorophenol. [5] The guppies that were exposed to this chemical were more likely to be eaten due to their slower responses. This is another example of a behavioral sublethal effect that leads to ecological death.

Copper

An effect caused by copper is impacting the salmon olfactory system. The olfactory system is used to gather important information about one's environment. In the case of salmon, olfactory cues can gather information about habitat quality, predators, mates and more. [6] Salmon can detect distinct copper gradients using their olfactory system, and use this information to avoid contaminated waters. [6] However, when salmon are affected by copper, the olfactory system can be impacted in a matter of minutes. [6] If the fish is no longer able to gather environmental information, it may be at risk for predation or unable to find resources for survival. This is an example of a physiological sublethal effect leading to ecological death.

Related Research Articles

Toxicity The ability of a chemical to cause damage to life

Toxicity is the degree to which a chemical substance or a particular mixture of substances can damage an organism. Toxicity can refer to the effect on a whole organism, such as an animal, bacterium, or plant, as well as the effect on a substructure of the organism, such as a cell (cytotoxicity) or an organ such as the liver (hepatotoxicity). By extension, the word may be metaphorically used to describe toxic effects on larger and more complex groups, such as the family unit or society at large. Sometimes the word is more or less synonymous with poisoning in everyday usage.

Chronic toxicity, the development of adverse effects as a result of long term exposure to a contaminant or other stressor, is an important aspect of aquatic toxicology. Adverse effects associated with chronic toxicity can be directly lethal but are more commonly sublethal, including changes in growth, reproduction, or behavior. Chronic toxicity is in contrast to acute toxicity, which occurs over a shorter period of time to higher concentrations. Various toxicity tests can be performed to assess the chronic toxicity of different contaminants, and usually last at least 10% of an organism’s lifespan. Results of aquatic chronic toxicity tests can be used to determine water quality guidelines and regulations for protection of aquatic organisms.

Aquatic toxicology

Aquatic toxicology is the study of the effects of manufactured chemicals and other anthropogenic and natural materials and activities on aquatic organisms at various levels of organization, from subcellular through individual organisms to communities and ecosystems. Aquatic toxicology is a multidisciplinary field which integrates toxicology, aquatic ecology and aquatic chemistry.

Ecotoxicology is the study of the effects of toxic chemicals on biological organisms, especially at the population, community, ecosystem, and biosphere levels. Ecotoxicology is a multidisciplinary field, which integrates toxicology and ecology.

A toxicant is any toxic substance. Toxicants can be poisonous and they may be man-made or naturally occurring. In contrast, a toxin is a poison produced naturally by an organism. The different types of toxicants can be found in the air, soil, water, or food.

Ecotoxicity potential for biological, chemical or physical stressors to affect ecosystems

Ecotoxicity, the subject of study of the field of ecotoxicology, refers to the potential for biological, chemical or physical stressors to affect ecosystems. Such stressors might occur in the natural environment at densities, concentrations or levels high enough to disrupt the natural biochemistry, physiology, behavior and interactions of the living organisms that comprise the ecosystem.

Environmental toxicology multidisciplinary field of science

Environmental toxicology is a multidisciplinary field of science concerned with the study of the harmful effects of various chemical, biological and physical agents on living organisms. Ecotoxicology is a subdiscipline of environmental toxicology concerned with studying the harmful effects of toxicants at the population and ecosystem levels.

Environmental impact of pesticides

The impact of pesticides consists of the effects of pesticides on non-target species. Pesticides are chemical preparations used to kill fungal or animal pests. Over 98% of sprayed insecticides and 95% of herbicides reach a destination other than their target species, because they are sprayed or spread across entire agricultural fields. Runoff can carry pesticides into aquatic environments while wind can carry them to other fields, grazing areas, human settlements and undeveloped areas, potentially affecting other species. Other problems emerge from poor production, transport and storage practices. Over time, repeated application increases pest resistance, while its effects on other species can facilitate the pest's resurgence.

Developmental toxicity toxicity as observed in the development of an organism

Developmental toxicity is any structural or functional alteration, reversible or irreversible, which interferes with homeostasis, normal growth, differentiation, development or behavior, and which is caused by environmental insult. It is the study of adverse effects on the development of the organism resulting from exposure to toxic agents before conception, during prenatal development, or post-natally until puberty. The substance that causes developmental toxicity from embryonic stage to birth is called teratogens. The effect of the developmental toxicants depends on the type of substance, dose and duration and time of exposure.

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 standpoint. 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.

Persistent, bioaccumulative and toxic substances (PBTs) are a class of compounds that have high resistance to degradation from abiotic and biotic factors, high mobility in the environment and high toxicity. Because of these factors PBTs have been observed to have a high order of bioaccumulation and biomagnification, very long retention times in various media, and widespread distribution across the globe. Majority of PBTs in the environment are either created through industry or are unintentional byproducts.

A mode of toxic action is a common set of physiological and behavioral signs that characterize a type of adverse biological response. A mode of action should not be confused with mechanism of action, which refer to the biochemical processes underlying a given mode of action. Modes of toxic action are important, widely used tools in ecotoxicology and aquatic toxicology because they classify toxicants or pollutants according to their type of toxic action. There are two major types of modes of toxic action: non-specific acting toxicants and specific acting toxicants. Non-specific acting toxicants are those that produce narcosis, while specific acting toxicants are those that are non-narcotic and that produce a specific action at a specific target site.

Fish acute toxicity syndrome (FATS) is a set of common chemical and functional responses in fish resulting from a short-term, acute exposure to a lethal concentration of a toxicant, a chemical or material that can produce an unfavorable effect in a living organism. By definition, modes of action are characterized by FATS because the combination of common responses that represent each fish acute toxicity syndrome characterize an adverse biological effect. Therefore, toxicants that have the same mode of action elicit similar sets of responses in the organism and can be classified by the same fish acute toxicity syndrome.

Tissue residue is the concentration of a chemical or compound in an organism's tissue or in a portion of an organism's tissue. Tissue residue is used in aquatic toxicology to help determine the fate of chemicals in aquatic systems, bioaccumulation of a substance, or bioavailability of a substance, account for multiple routes of exposure, and address an organism's exposure to chemical mixtures. A tissue residue approach to toxicity testing is considered a more direct and less variable measure of chemical exposure and is less dependent on external environmental factors than measuring the concentration of a chemical in the exposure media.

Toxicodynamics, termed pharmacodynamics in pharmacology, describes the dynamic interactions of a toxicant with a biological target and its biological effects. A biological target, also known as the site of action, can be binding proteins, ion channels, DNA, or a variety of other receptors. When a toxicant enters an organism, it can interact with these receptors and produce structural or functional alterations. The mechanism of action of the toxicant, as determined by a toxicant’s chemical properties, will determine what receptors are targeted and the overall toxic effect at the cellular level and organismal level.

Pre-spawn mortality is a phenomenon where adult coho salmon, Oncorhynchus kisutch, die before spawning when returning to freshwater streams to spawn. It is also known as Urban Runoff Mortality Syndrome in more recent studies. This occurrence has been observed in much of the Puget Sound region of the Pacific Northwest. During fall migration, salmonids pass through urban watersheds which are contaminated with stormwater runoff. As the coho salmon pass through these waters, many will show symptoms of lethargy, loss of equilibrium and disorientation, and die within a few hours of showing these symptoms. These symptoms and behaviors are prevalent after rain events. Mortality often occurs before salmon have the opportunity to spawn, which is determined by cutting open female carcasses and observing for unfertilized eggs. Rates of pre-spawn mortality could impact the local salmon populations. Based on model projections, if rates continue, populations of coho salmon could become extinct within the next few decades.

An early life stage (ELS) test is a chronic toxicity test using sensitive early life stages like embryos or larvae to predict the effects of toxicants on organisms. ELS tests were developed to be quicker and more cost-efficient than full life-cycle tests, taking on average 1–5 months to complete compared to 6–12 months for a life-cycle test. They are commonly used in aquatic toxicology, particularly with fish. Growth and survival are the typically measured endpoints, for which a Maximum Acceptable Toxicant Concentration (MATC) can be estimated. ELS tests allow for the testing of fish species that otherwise could not be studied due to length of life, spawning requirements, or size. ELS tests are used as part of environmental risk assessments by regulatory agencies including the U.S. Environmental Protection Agency (EPA) and Environment Canada, as well as the Organisation for Economic Co-operation and Development (OECD).

The olfactory system is the system related to the sense of smell (olfaction). Many fish activities are dependent on olfaction, such as: mating, discriminating kin, avoiding predators, locating food, contaminant avoidance, imprinting and homing. These activities are referred to as “olfactory-mediated.” Impairment of the olfactory system threatens survival and has been used as an ecologically relevant sub-lethal toxicological endpoint for fish within studies. Olfactory information is received by sensory neurons, like the olfactory nerve, that are in a covered cavity separated from the aquatic environment by mucus. Since they are in almost direct contact with the surrounding environment, these neurons are vulnerable to environmental changes. Fish can detect natural chemical cues in aquatic environments at concentrations as low as parts per billion (ppb) or parts per trillion (ppt).

In aquatic toxicology, the sediment quality triad (SQT) approach has been used as an assessment tool to evaluate the extent of sediment degradation resulting from contaminants released due to human activity present in aquatic environments. This evaluation focuses on three main components: 1.) sediment chemistry, 2.) sediment toxicity tests using aquatic organisms, and 3.) the field effects on the benthic organisms. Often used in risk assessment, the combination of three lines of evidence can lead to a comprehensive understanding of the possible effects to the aquatic community. Although the SQT approach does not provide a cause-and-effect relationship linking concentrations of individual chemicals to adverse biological effects, it does provide an assessment of sediment quality commonly used to explain sediment characteristics quantitatively. The information provided by each portion of the SQT is unique and complementary, and the combination of these portions is necessary because no single characteristic provides comprehensive information regarding a specific site

Toxicological databases are large compilations of data derived from aquatic and environmental toxicity studies. Data is aggregated from a large number of individual studies in which toxic effects upon aquatic and terrestrial organisms have been determined for different chemicals. These databases are then used by toxicologists, chemists, regulatory agencies and scientists to investigate and predict the likelihood that an organic or inorganic chemical will cause an adverse effect on exposed organisms.

References

  1. 1 2 3 4 Scott, G.R., and K.A. Sloman. 2004. The effects of environmental pollutants on complex fish behavior: integrating behavioural and physiological indicators of toxicity. Aquatic Toxicology 68:369-392.
  2. 1 2 3 4 5 6 7 8 Rand, G.M. (Ed). Fundamentals of Aquatic Toxicology: Effects, Environmental Fate, and Risk Assessment. 2nd Ed. Florida: CRC Press, 1995.
  3. 1 2 3 U.S. Dept. of Interior, National Biological Service. “Environmental Contaminants”. Status and Trends of the Nation’s Biological Resources. Dept. of Interior, National Biological Service: Washington, DC. 1998. <http://www.nwrc.usgs.gov/sandt/> 15 May 2013.
  4. Scholz, N.L., Truelove, N.K., French, B.L., Berejikian, B.A., Quinn, T.P., Casillas, E., Collier, T.K. 2000. Diazinon disrupts antipredator and homing behaviors in Chinook salmon (Oncorhynchus tshawytschaI). Can. J. Fish. Aquat. Sci. 57: 1911-1918.
  5. 1 2 Brown, J.A., Johansen, P.H., Colgan, P.W., Mathers, R.A. 1985. Changes in the predator-avoidance behavior of juvenile guppies (Poecilia reticulata) exposed to pentachlorophenol. Can. J. Zool. 63: 2001-2005.
  6. 1 2 3 Baldwin, D.H., Sandahl, J.F., Labenia, J.S., Scholz, N.L. 2003. Sublethal effects of copper on Coho Salmon: Impacts on nonoverlapping receptor pathways in the peripheral olfactory nervous system. Environ. Tox. and Chem. 22(10):2266-2274.

See also