Freedman defines a pollutant as “the occurrence of toxic substances or energy in a larger quality then the ecological communities or particular species can tolerate without suffering measurable detriment” (Freeman, 562). Although the effects of a pollutant on an organism vary depending on the dose and duration (how long administered). The impact can be one of sublethality to lethality, all dependent upon the factors involved. These factors need to be looked at when determining an ecosystem’s disturbance by a pollutant. Some of the most frequent pollutants in our ecosystem include: gases such as sulphur dioxide, elements such as mercury and arsenic, and even pollution by nutrients which is referred to as eutrophication. Each of these pollutants pose a different effect on the ecosystem at different doses.
This varied effect is what is referred to as dose and duration. The amount of the pollutant administered over what period of time greatly affects the impact that the pollutant will have on an ecosystem and population. Pollutants can affect both a population and an ecosystem. A pollutant on a population level can be either non-target or target. Target effects are those that can kill off the entire population. Non-target effects are those that effects a significant number of individuals and spreads over to other individuals, such is the case when crop dusters spread herbicides, insecticides. Next we look at population damage by a pollutant, which in turn has a detrimental effect on the ecosystem in several ways. First, by the killing of an entire population by a pollutant, it offsets the food chain and potentially kills off other species that depended on that organism for food. Such is the case when a keystone species is killed.
If predators were the dominant species high on the food chain, the organisms that the predator keep to a minimum could massively over produce creating a disturbance in the delicate balance of carrying capacity in the ecosystem. Along with this imbalance another potential problem in an ecosystem is the possibility of the pollutant accumulating in the (lipophilic) fat cells. As the pollutant makes it way through the food chain it increases with the increasing body mass of the organism. These potential problems are referred to as bioconcentration and biomagnificaiton, respectively. Both of these problems being a great concern of humans because of their location on the food chain. These are only a few of the impacts that a pollutant can have on a population and ecosystem.
Another factor to consider is the carrying capacity when evaluating the effects of a pollutant on an ecosystem. A carrying capacity curve describes the number of individuals that a specific ecosystem can sustain. Factors involved include available resources (food, water, etc.), other members of the species of reproductive age and abiotic factors such as climate, terrain are all determinants of carrying capacity. This curve is drawn below: # of individuals Years If a pollutant is introduced into an ecosystem , it can affect the carrying capacity curve of several organisms (Chiras, 127). This effect on the curve is caused by the killing off of the intolerant and allowing more room for both the resistant strain and new organisms. In some cases the pollutant will create unsuitable habitats causing migration. Another important part of the idea of a carrying capacity is the Verholst (logistic) equation: The actual growth rate is equal to the potential growth rate multiplied by the carrying capacity level.
Three major characteristics exist for this equation. First, that the rate of growth is density dependent, the larger the population, the slower it will grow. Secondly, the population growth is not limited and will reach a stable maximum. Lastly, the speed at which a population approaches its maximum value is solely determined by the rate of increase (r). In a population with a stable age structure this would be the birth rate minus the death rate, but this is almost impossible. If any of the variables in this equation are affected by a pollutant then the growth rate of an organism can be seriously affected which can in turn affect the entire ecosystem (Freeman, 122). Now using the approach of classical toxicology we study the poisoning effects of chemicals on individual animals resulting in lethal or sublethal effects.
Effects on individuals may range from rapid death (lethal) through sublethal effects to no effects at all. The most obvious effect of exposure to a pollutant is rapid death and it is common practice to assess this type of toxicity by the LD50 (the lethal dose for 50% of test animals) values, scientist can judge the relative toxicity of two chemicals. For example, a chemical with an LD50 of 200 milligrams per kilogram of body weight is half as toxic as one with an LD50 the more toxic a chemical. Death is rarely instantaneous, and even cyanide takes at least some tens of seconds to kill a human being. Death is alwaBAD BAD BAD BAD BAD BAD BAD BAD BAD BAD BAD BAD BAD BAD BAD BAD one set of conditions, often ill defined, with one type of exposure, and with no indication of the influence of other environmental variables.
Perkins (1979) suggests that a sublethal exposure kills at most only a small proportion of a population, but the possibility that s sublethal exposure could cause a small proportion of individuals to die from acute toxicity seems self contradictory (Freedman, 126). For both the sake of this assignment and for practical purposes, it would be incautious to suppose that a sublethal exposure that affects individual organisms adversely is not close to that which will affect the population. There is no good reason to suppose that there is a constant relationship for different pollutants or different species, between the dose needed to kill and that needed to impair an organism.
Therefore, given the difficulties of studying an ecosystem, the most effective way to predict biological effects is likely to be by discerning the least exposure that produces a deleterious response in individual organisms (Moriarty, 1960) and then examining the extent to which different environmental conditions alter this minimum exposure. Further adding to the complexity several additional factors come into play with the effect and response of an organism from a pollutant. One such factor is age. Although we think of youngsters of all species as resilient creatures, young, growing organisms are generally more susceptible to toxic chemicals than adults (Chiras, 127). Health Status is determined by many factors, among them one’s nutrition, level of stress, and personal habits such as smoking.
As a rule, the poorer one’s health, the more susceptible he or she is to a toxin (Freeman, 214). Toxins may also interact with each other producing several different responses. Some chemical substances for example, team up to produce an additive response that is, an effect that is simply the sum of the individual responses. Others may produce a synergistic response that is, a response stronger than the sum of the two individual ones. A pollutant can also synergize for instance, sulphur dioxide gas and particulates (minute airborne particles) inhaledtogether can reduce air flow through the lungs’ tiny passages. The combined response is much greater than the sum of the individual responses. Plants have three strategies in response to a disturbance – this was suggested by Grimes. These strategies are: C – selection – having high competitive ability S – selection – having a high endurance for stress R – selection – having a good ability to colonize disturbed areas.
Plant response to a disturbance was suggested by Connell and Slatyer (1977) using models. Model I (the “facilitation” model assumes that only certain species that come early in the succession are capable of colonizing the site. In contrast the other two models both assume that any individual of any species that happens to arrive at the site is capable of colonizing it, although all models accept that certain species will tend to appear first because of their colonizing abilities. All models also suppose that the first colonist will so modify the site that it becomes unsuitable for those species that normally occur early in the succession. The three hypotheses then suggest three different ways in which other species will appear. Model I suggests that early occupants modify the environment so that it becomes more suitable for species that come later in the succession. Model II (the “tolerance” model) suggests that the sequence in which species appear depends solely on their speeds of dispersal and growth.
Model III (inhibition) – the species already present makes the environment less suitable for subsequent recruitment of later species. All these hypothesis do not rely on the idea of a community as a sugra-organism but on succession as a sugra-organism but on succession as a process that relies on two factors: 1) the probabilities that propagules of different species will be present and 2) the ability of these propagules to survive, develop and reproduce. Now to look at the whole picture, we ask ourselves: “How do we predict the response of a community from a pollutant?” Should we look at one population at a time, or in some holistic approach. Moriarty suggests that some of the currently favored approaches rest ont he assumption, often implicit rather than explicit, that communities are sugra-organisms.
He (Moriarty) suggests that two topics that should be discussed when dealing with the idea of community response: 1) indicator species 2) biological or environmental health may be misleading. The term indicator species, which is used in the classification of communities (p. 62) is also used in ecotoxicology, with a variety of meanings. At times it indicates the idea that knowledge of one species within a community will indicate the well-being or biological health of the whole community. Moriarty suggests that this seems a reasonable proposition if one accepts the traditional view of community as sugra-organism, but suggests that it is in fact misleading.
He (Moriarty) adds that there is no fundamental reason from community structure to suppose that any particular species within the community will give a better measure of impact from pollutants than will another. Pollutants will affect populations of particular species, and which species are first affected will depend on the relative degrees of exposure and susceptibility and these are functions much more of the particular pollutant and of the individual species than of the community. An indicator species can only be used to assess the impact of pollution on a community if quite a lot is known about both the pollution and the community (Moriarty, 69). Concerning the idea of the concept of biological or environmental health being misleading: one may properly refer to the health of a community.
A community can change “markedly” if affected by a pollutant, but it will just become a different community that is neither more nor less “healthy” just different (Moriarty, 69). It may be a less desirable community, for economic, social, scientific or aesthetic reasons, but that is quite a different matter. Effects of pollution may be described as a retrogression – a decrease in diversity, productivity, biomass and structural complexity. Moriarty argues that while there may be the appearance of a retrogression process it should not be taken as a generality. In conclusion, on the effect and response of an organism from a pollutant, the most appropriate emphasis is on populations. The effect of pollutants on populations within a community can be complex and apart from reduction or elimination of populations – resurgence, population increase or introduction of rarer species, sublethal effects and genetic changes may all be part of the changes that occur.
Another very important characteristic of populations that we cannot overlook is their emetic composition. Much of the variation between individuals is inherited from their parents. It is common knowledge that relatively few offspring of any species survive to reproduce. Charles Darwin (biologist, 1859) formed the idea of natural selection: the idea that some individuals will have a higher probability of survival than others, and on average such individuals will then leave more descendants than other less well adapted individuals. We will use Darwin’s, Mendel’s and Watson and Crick’s and other information to investigate our concern – the role of pollutants in natural selection.
It has been shown many times that pollutants can exert powerful selective forces, and we need therefore to understand something of the mechanisms of inheritance and how natural selection acts on populations. For the purpose of this assignment I will outline/review all the general findings of important works that proved significant in understanding the concepts of genetics. A good place to start would be with an outline of some of Mendel’s results obtained when breeding peas (Pisum sativum). “A” indicates the dominate gene for yellow seed, “a” the recessive gene for green seed. However, genes do not always fall into this simple dominant/recessive pattern. Some may be incompletely dominant in the heterozygote, showing a transition stage between the phenotypes of the homozygous dominant and recessive conditions. Later workers also found that there are often more than two alternative forms alleles) of a gene.
One such worker was Avery (1944) who showed that the genetic material in a bacterium consists of the nucleic acid DNA (deoxyribonucleic acid), and in 1953 Watson and Crick first suggested the three-dimensional structure of DNA from which has developed all the subsequent work on the genetic code. The essential feature of this code is that: genes are arranged along chromosomes, which in essence may be regarded as giant molecules of DNA. The DNA molecule consists of two intertwined helical chains of many nucleotides, with ten nucleotides in both chains for each complete turn of the helix (Watson, 1965). Diagram to illustrate the double helix of DNA with the two polynucleotide chains linked by complementary base-pairs (Adenine (A) with Thymine (T), and Guanine (G) with Cytosive (C).
Replication occurs when the two strands separate and both act as templates on which new complementary strands are formed (Moriarty, 62). Occasionally, something goes wrong with the replication process and one or more genes may be altered, lost or gained. These changes, or mutations are usually less favorable to the organism than the original gene, and are often sufficiently unfavorable to be lethal. Nevertheless, mutations in the reproductive cells are of crucial importance: these are in favorable, the source of new genetic variation in subsequent generations. This knowledge about gene structure and function modifies the Mendelian view of inheritance. Now, after the brief introduction and history of genetics it is time to consider the relevance of ecological genetics to pollution. Most current problems of pollution occur on a much shorter time-scale than that required for the evolution of new species.
The critical difference between evolutionary change and that wrought by pollution is the speed: populations can disappear very rapidly from pollution and if unchecked, we would have a very impoverished fauna and flora (Moriarty, 81). One very popular example of the effects of pollution on wildlife, and perhaps the most striking evolutionary change over to be actually witnessed was the occurrence of melanism in moths. This effect is commonly associated with industrial development. White moths would rest on white lichen on trees and were well-nigh visible on them. But with industrial pollution (between 1848 and 1990) lichen turned a black color exposing and making the white moth (f. typica) prey to birds. Birds posed a selective pressure against the white moths. Now black moths were favored evolutionary. This is known as the heterozygous advantage, in which a bank of recessive alleles becomes favored due to a change in the environment.
The biological significance of melanism was a matter for debate for some decades, and although it is now generally accepted that melanism in (f. typica) is associated with atmospheric pollution, some of the details are still unclear. Although several points are worth emphasizing. Pollution in this instance is not having a direct effect on the moth populations, nor indeed on their predators, but an alteration to the habitat has altered greatly the relative fitness of different genotypes. Melanism also illustrates the difficulty of producing adequate proof, or disproof, of cause and effect when pollutants are thought to be causing major biological effects. In conclusion, with regards to genetics, it is important to appreciate that the effects of pollutants can be modified by an organisms genetic constitution, and that pollutants can alter a population’s gene pool (Freeman, 128).
The interactions between pollutants and genes can be relevant both to understanding and to predicting effects and are potentially of great value for monitoring (Moriarty, 102). In summary, as stated throughout this school year in my 2375 Pollution class, the effects of pollutants on populations are mediated via their effects, direct or indirect on individuals and the likelihood of these effects depends on the dose. Sublethal effects can be unravelled from knowledge of the mode of action. Alternatively, emphasis in the study of sublethal effects can be placed on the health of the individual organism. With both approaches, the effect of other environmental variables needs to be given much more prominence than heretofore and this could profitably be linked with studies on amounts of pollutant within organisms (Moriarty, 176).
It is from this basis that Moriarty states that we have to consider how best to predict and to monitor the ecological effects of potential pollutants. In my opinion, I feel that (as does Moriarty) one should relate pollution to the wider aspects of man’s impact on his environment. We can, to a considerable extent, control and mitigate our negative impacts upon this planet because as we have learned from our past experiences, this planet does have a finite carrying capacity for our own as well as for all other species.
Campbell, N.A. Biology (3rd ed) 1993. Benjamin/Cummings Publishing Company. Chiras, Daniel D. Environmental Science: Action for a Sustainable Future. (4th ed), 1994. The Benjamin/Cummings Publishing Company. Freedman, Bill. Environmental Ecology: The Ecological Effects of pollution, disturbances and other stresses / Bill Freedman (2nd ed.), 1995. Moriarty, F. Ecotoxicology (2nd ed), 1993. Academic Press Limited.