QuestionQUESTION: dear to whom this may concern,
how do different pesticides affect the health/growth of grass/plants? I am doing a science fair project and i would like to see what a person who studies this thinks about what happens to the plants/grass. ok for my science project i probably will be testing diferent types of pesticides on grass and see what different kinds and amounts will do to the plants.
thanks so much for your help,
shira johnston (8th grade)
ANSWER: Hi there. Before we start keep in mind that pesticides include amy material that is used to get rid of pests. Pests are any unwanted thing. For example: insects,mammals and weeds. Just to name a few. Below is a very extensive article. I hope you can understand it.
If not let me know Ans will try to find something less technical. Thanks,Bill
Methods to Assess Adverse Effects of Pesticides on Non-target Organisms
14.1 INTRODUCTION
14.2 MEASURING PESTICIDE-INDUCED TOXICITY IN PLANTS
14.2.1 PLANTS IN THE FIELD AND IN NATURAL COMMUNITIES
14.2.2 PLANTS IN GREENHOUSES AND GROWTH CHAMBERS
14.2.3 PLANT TISSUE CULTURES
14.3 DETECTING GENOTOXIC EFFECTS OF PESTICIDES IN PLANTS
14.3.1 CYTOGENETIC ASSAYS
14.3.2 ASSAYS FOR DETECTION OF GENE MUTATIONS
14.3.3 DETECTION OF GENOTOXIC METABOLITES FORMED IN PLANTS FROM PESTICIDES
14.4 CONCLUSIONS
14.1 INTRODUCTION
Plants are the main recipients of pesticides, regardless of whether they themselves represent the target organism (e.g., weed) or whether the targets are pests, pathogenic fungi, etc. They are exposed to pesticides from direct application, through the uptake from soil and water, and from atmospheric drift. It has been shown (Ware et al., 1970) that about half of pesticides applied by aircraft land outside the target cropland or forest and fall out either on adjoining ecosystems or drift into distant ecosystems.
Pesticides tend to be very reactive, mostly electrophilic, compounds that can react with various nucleophilic centres of cellular biomolecules, including DNA (Crosby, 1982), or form even more reactive electrophilic products that either modify cellular components or are metabolized to more or less stable products. Ideally, pesticides should affect only the target organism; however, this ideal is rarely attained because of similarities in the basic life processes of both target and non-target plants. Toxicity, including mutagenicity, is the consequence; it is mediated by various changes in the metabolism of plants, including formation of metabolic pathways of pesticide degradation.
Differential sensitivity of plant species to toxic and genotoxic effects of pesticides has been shown to cause overall changes in species ratios, both among weeds in a crop field and in natural plant communities, due to the reduced abundance of susceptible species with concurrent increases in naturally tolerant species. This may have further consequences for the entire ecosystem (Pimentel and Edwards, 1982). An important factor in this situation is the occurrence of herbicide-resistant forms within susceptible plant species. Here, pesticides can play roles as agents favouring the selection of pre-existing resistant mutants and as potential inducers of genetic changes (Grant, 1972, 1982a; Brown, this volume). Genotoxic pesticides are potentially able to increase mutations in DNA, controlling the expression of various qualitative and quantitative traits that could cause genetic instabilities of natural plant populations and in crop varieties (Crosby, 1982).
Another important consideration is the possible formation of stable metabolites and their accumulation in plants to such an extent that they can become harmful to both human and animal populations via their respective food chains. Attention must be given to this problem despite the observation that bound residues incorporated into lignin, hemicellulose, and other carbohydrate components of the cell wall of plants are generally considered to be less toxic to the biosphere than corresponding adducts produced in animal cells (Lamoureux and Rusness, 1986).
Pesticides have also produced changes in plant metabolism and in nutritional patterns that may have secondary effects on the ecology. Even when applied at recommended dosages, some herbicides have been found to increase unwanted insects and plant pathogens (Pimentel, 1971; Oka and Pimentel, 1974). For example, when corn was treated with 2,4-dichlorophenoxyacetate (2,4-D) at the recommended dosage of 1 kg/ha, the numbers of corn leaf aphids increased by threefold; corn borers were 26 per cent more abundant and were also 33 per cent larger than the same insects on untreated corn (Oka and Pimentel,1974). The larger size corn borers produced one third more eggs, and thus contributed to the overall build-up of corn borers in corn fields.
The insecticides monocrotophos and phosphamidon likewise increased concentrations of nitrogen and phosphorus in rice plants; these changes were thought to contribute to a resurgence in numbers of the rice blue leafhopper (Mani and Jayraj, 1976). In addition to the increased number of plant insect pests, herbicides can also increase plant pathogen attack. For instance, when corn was treated with a recommended dosage of 2,4-D (1 kg/ha), black corn smut grew fivefold larger than on untreated corn (Oka and Pimentel, 1974). Also, corn treated with 2,4-D and resistant to southern corn leaf-blight lost its resistance to the blight.
Increasing insect pest and plant pathogen attacks on crops due to the use of some herbicides may in turn increase the application of more pesticides, such as insecticides and fungicides. Thus, the environmental problem in using herbicides may be amplified beyond that of the herbicide itself.
Most nutrients, especially C, K, N, P, and S, are taken up by plants, which in turn may be eaten by animals. These nutrients are eventually returned to the soil or atmosphere via decomposition of decaying organisms. The amounts and forms of nutrients in soil and plants may be changed by pesticides affecting the dynamics of these animal in the ecosystem.
Pesticides can alter the chemical composition of plants. The changes that occur appear to be specific for both the plant and the pesticides involved. For example, certain organochlorine insecticides have increased the amounts of some macro- and micro-element constituents (Al, B, Ca, Cu, Fe, K, Mg, Mn, N, P, Sr, and Zn) of corn and beans, and decreased the amounts of others (Cole et al., 1968). In another study, DDT, aldrin, endrin, and lindane were found to stimulate synthesis of the important amino acids arginine, histidine, leucine, lysine, proline, and tyrosine in corn, but decreased the content of tryptophane (Thakre and Saxena, 1972). The herbicide simazine increased water and nitrate uptake in barley, rye, and oat seedlings, resulting in increased plant weight and total protein content (Ries and Wert,1972). Soil treatment of carrot with insecticides Nexion, Birlane, and Dyfonate increased the concentration of free sugars in roots, whereas an opposite effect was observed after the action of the herbicide Dosanex (Rouchaud et al., 1983).
In this chapter attention is paid mostly to the methods and experimental approaches suitable for detection of immediate and delayed toxicity of pesticides, their harmful metabolites and residues on plants. The chapter does not describe all methods used to measure pesticide metabolites and residues, changes in the plant metabolism, or nutritional requirements caused by pesticides.
14.2 MEASURING PESTICIDE-INDUCED TOXICITY IN PLANTS
The toxic effects of pesticides accumulated in soil or water can be measured on intact plants grown in the natural communities or in the field, on intact plants cultivated in the greenhouse or growth chambers, or on plant cell cultures in vitro.
14.2.1 PLANTS IN THE FIELD AND IN NATURAL COMMUNITIES
Several endpoints are available to measure an immediate toxic effect of pesticides on crop plants in the field. Standardized procedures in field trials simulating the conditions of agricultural utilization exist, and are recommended by authorities for evaluation of toxic effects of pesticides, especially herbicides, on crops. They measure toxicity to the target organism and to crops by using endpoints such as plant emergence or seed germination, crop stand or survival, growth rate, various types of injury during plant growth (e.g., chlorosis), seed setting fresh or dry weight of plants at harvest, and crop yield. Data from these trials may serve to decide suitable doses of pesticides in fields to avoid harmful effects on crop species or varieties under specific climatic conditions (Frans et al., 1988).
Similar experimental protocols can be followed for studies dealing with quantitative and qualitative changes caused by herbicides among weed species in crop fields and among those in natural plant communities on roadsides, grasslands, and forests (Way and Chancellor, 1976). The experimental territory is to be divided into standard plots exposed to a test herbicide or a mixture of herbicides and to untreated plots as controls. In each plot, individual species and the number of individuals within each species are determined before the application of pesticides and at various times during and after pesticide application. Finally, plants are harvested; various endpoints are measured separately according to species and plots. Survival to harvest, dry or wet weight of plants or their parts, and seed setting or seed weight can be measured and statistically analysed using principal-component analysis or linear regression modelling (Tomkins and Grant, 1974, 1976; Campbell et al., 1981)
In general, herbicides in experiments lasting even several years do not eradicate susceptible species, but rather reduce their abundance. With reductions in susceptible species, a concurrent increase in species naturally tolerant to the tested compound(s) is typical. This situation results in an overall change in species ratios, but with no change in the number of species present (Chancellor, 1979). For instance, in plots sprayed annually with 2,4-D for 36 years, no new major species has become established (Hume, 1987).
14.2.2 PLANTS IN GREENHOUSES AND GROWTH CHAMBERS
Greenhouse and growth-chamber conditions are especially suitable for determining the importance of individual external factors like temperature, light intensity and quality, day length, water stress, nutrition, and air humidity on the uptake, absorption, transport, translocation, metabolism, persistence, disappearance and overall toxicity of pesticides in the whole plants (Cole, 1983; Lamoureux and Rusness, 1986).
Greenhouse or growth-chamber toxicity tests on individual plant species are often used as bioassays to detect pesticides residues in soil or to assay herbicide toxicity on crop plants, but these tests can be applied to all other studies of pesticide-plant interactions. The tests are simple, rapid, and highly standardized with regard to number of plants per dose of pesticide, stage of plant development, dose range and number of repetitions, conditions of plant cultivation, positive and negative controls, and handling of data.
Principally, they follow techniques of classical growth analysis (Evans, 1972; Cartwright, 1976), but various protocols are available for different testing purposes (Hance and McKone, 1976; Horowitz, 1976; Banki, 1978; Nyffeler et al., 1982). Pesticides are applied to soil or sprayed on seedlings, and their effects are measured mostly by the wet or dry weight of either the whole plant or separate shoots, roots, and leaves. Toxic effects are usually expressed by constants like LD50 or ED50 that correspond to the pesticide concentration causing 50 per cent plant death or 50 per cent reduction in plant growth or weight compared to untreated controls (Hance and McKone, 1976).
14.2.3 PLANT TISSUE CULTURES
Plant tissue cultures are used increasingly in pesticide studies to screen new compounds, understand the mechanism(s) of pesticide action, bioassay metabolites, ensure experiments without microbial contamination, and save time and reduce costs. Cells in cultures rapidly absorb chemicals with which they come into contact, can be maintained for a long time, and have a high rate of metabolite formation; experiments can be standardized to a greater extent with cultures than with intact plants; and metabolic products are easily isolated and separated. By contrast, plant tissue culture techniques in pesticide research are useless in evaluating contributions of plant-associated microorganisms or cuticular or vascular transport-mediated phytotoxicity or in testing for the phytotoxicity of herbicides acting as photosynthetic inhibitors, unless they produce additional toxic effects independent of the main pathway. Sufficient pieces of evidence are available indicating both similarities and differences in the response of plant tissue cultures and intact plants to pesticides (Mumma and Davidonis, 1983; Swisher, 1987; Gressel, 1987). Consequently, in vitro test results must be validated in whole plants.
Phytotoxicity of pesticides is measured either on calluses grown on agar solidified medium or on cell suspension cultures dispersed in liquid media. The suspension cultures are more capable of being standardized and tend to produce substantial reproducibility. Various simple and standard procedures can be recommended (Mumma and Davidonis,1983; Swisher, 1987; Langebartels and Harms, 1986). The toxicity of pesticides is estimated according to the depression of growth and vitality of cells or calluses. The simplest way is to measure the wet weight of calluses, packed volume of cell suspensions (determined after centrifugation in graduated tubes), or their settled volume (in nephelometric flasks). Commonly used methods include the determination of dry weight of cell suspension, measurement of cell number, optical density in sonicated cell suspension, electrical conductivity, permeability of fluorescein, reduction of triphenyltetrazolium chloride, and incorporation of 14C-leucine into proteins (Langebartels and Harms, 1986; Gressel, 1987; Swisher, 1987).
14.3 DETECTING GENOTOXIC EFFECTS OF PESTICIDES IN PLANTS
Genetic changes induced by pesticides, their metabolites, and residues are expressed by various endpoints, which include:
1.
Structural changes in chromosomes and chromatids, called chromosomal aberrations (breaks, deletions, inversions, gaps, translocations, rings) and other disturbances (stickiness, clumping, erosion)
2.
Disturbances in the mitotic or meiotic division, like spindle inactivation, causing so-called c-mitosis, non-disjunction, and other irregularities in the chromosome distribution during anaphase, resulting in polyploid or aneuploid cells
3.
Recombinational events like somatic crossing over and sister chromatid exchanges
4.
Sterility and embryonic lethality
5.
Mutations in somatic tissues expressed as sectors on leaves and flowers
6.
Mutation in generative cells expressed either on pollen grains (in haplophase) or in sexual progeny.
To determine these endpoints, a number of plant assays have been developed, based mostly on laboratory application with test compounds, followed by cultivation of plants or their parts (roots) in the laboratory, greenhouse or field. Only a few of them are suitable or have been adapted for testing genetic effects of pesticides in situ, under conditions of their utilization in agriculture, horticulture and forestry, or to assess exposures in natural plant communities (Grant, 1982a; Plewa, 1985; Ma and Harris, 1985). In addition, several plant assay systems frequently used for monitoring genotoxic substance in the air and water as a part of assessing risks to humans (Grant and Zura, 1982; Constantin, 1982) have been employed occasionally to test pesticides. As pointed out by Grant (1982a), over 230 plant species have been used in various studies on mutagenesis; however, only a limited number of plant assays are available for routine screening for genotoxicity of pesticides.
14.3.1 CYTOGENETIC ASSAYS
Assays for detection of chromosome aberrations in plants are some of the oldest, simplest, most reliable, and least expensive methods in the field of environmental mutagenesis. Cytogenetic abnormalities can be detected in mitotic and meiotic divisions. Analyses of somatic chromosome aberrations are carried out in cells of growing root tips, stem apexes, or in pollen tubes, whereas studies of meiosis are carried out with pollen mother cells (PMC). Most advantageous for cytogenetic analysis are the species having small numbers of morphologically distinguishable chromosomes that can be viewed microscopically by staining and preparation of squashed slides from soft meristematic tissues. These conditions are met in root tips of the broad bean Vicia faba (Kihlman and Anderson, 1984), onion Allium cepa (Grant, 1982b), hawks beard Crepis capillaris, pea Pisum sativum, in root tips and PMC of barley Hordeum vulgare, corn Zea mays, and spiderwort Tradescantia (Grant et al., 1981; Ma, 1982). This is the reason why these organisms have been used to test for clastogenicity of environmental mutagens, including pesticides. Techniques for staining and slide preparation are so universally known and relatively simple that many other species, including crop and wild plants, may be screened for cytogenetic changes induced by pesticides in situ or under laboratory conditions.
Two groups of cytogenetic tests are used in plants:
1.
Laboratory assays. These are characterized by a short-term (124 h) application of test pesticides on seeds or root tips, often at higher doses than used in agriculture, horticulture, or forestry. The evaluation of chromosomal structural changes is performed during the first cell cycle after pesticide application. Mostly Vicia faba, Allium cepa, and barley root tips or seeds are used for this assay.
2.
In situ assays. They enable application of pesticides under conditions and stage of plant development similar to that in agricultural practice. Experiments of this type can be carried out under field conditions using plants of a single species (mostly barley, corn, Vicia faba) or multiple species forming the components of natural plant communities.
Experiments of this type have been carried out by Tomkins and Grant (1974, 1976; Grant and Zura, 1982), who analysed 12 different species among 50 detected in experimental plots on roadsides close to agricultural fields. Plants in these plots were sprayed with selected herbicides (picloram, simazine, and diurone) at doses used in agriculture, and their cytogenetic effects were determined in somatic and meiotic cells of flower buds collected at different sampling periods. The researchers observed a significant but differential increase in the frequency of aberrant cells in various species, the highest being in the mid-season of spraying (June and July) and the lowest in the off-season.
Two other types of rapid and efficient assays in plants do not detect the cytogenetic damage itself, but rather its consequences: formation of micronuclei, and pollen abortion of sterility and lowered seed setting.
The micronucleus test in Tradescantia is based on the fact that this organism's chromosomes in early meiotic prophase are extremely prone to breakage; and, subsequently, acentric fragments lead to formation of micronuclei in the tetrade stage of pollen development. Ma (1982) has developed a sensitive assay for scoring micronuclei in flower bud cells after exposition of inflorescences to gaseous or liquid forms of environmental pollutants. The assay is very rapid, because the number of micronuclei can be determined 2430 h after the action of the tested compound. A special vegetatively propagated clone of Tradescantia paludosa, recommended for the assay, can be transferred to the exposed area either as cuttings or as plants in pots. This assay has been applied also for fumigants and several pesticides in the liquid form (Ma et al., 1984).
Reduced pollen fertility and seed setting are assumed to be consequences of chromosome aberrations induced in the meiotic stage. Indeed, pesticides that induce chromosome aberrations in meiosis also reduce pollen viability (Grant, 1982a).
The pollen sterility assay can be explored for studies in natural plant communities. This kind of research may follow the protocol described by Kurinnyj (1983), based on random sampling of flowers of various species in areas exposed to pesticides and detection of pollen viability by acetocarmine squash technique or by fluorescence techniques.
Several test systems in plants are suitable for detection of gene mutations either in many (multiple loci systems) or in one or two specific gene markers (specific locus systems). Mutations are expressed as hereditary changes in the phenotypes observed in haplophase (pollen grains), in somatic tissues of the exposed plants or in the sexual progeny of exposed plants (where mutations of a recessive character are induced in the germ cells of self-pollinated plants).
14.3.2 ASSAYS FOR DETECTION OF GENE MUTATIONS
Multiple-loci system tests are very sensitive, because a variety of genetic events in a large number of loci are measured. In the most frequently used systems (i.e., in barley and Arabidopsis thaliana), based on determination of chlorophyll and/or embryonic recessive lethals, 700800 loci are involved (Nilan, 1978). The multilocus system tests in plants are comparable to the Drosophila mutation assay, and are considered to be more relevant than specific-locus system tests for prediction of mutagenic response in people. Both in barley and in Arabidopsis thaliana, test compounds are usually applied in liquid form on seeds, and the mutations are evaluated after self-pollination and formation of seeds in plants grown in the greenhouse or in the field. Whereas in barley chlorophyll-deficient mutants are recognized at seedling stage in Arabidopsis they can be detected on unripe seeds in the siliquae (Grant et al., 1981; Redei et al., 1984). The Arabidopsis assay is much less time- and space-consuming, and cheaper than the barley assay. In both systems, a large number of mutagenic compounds, including pesticides, have been screened (Grant, 1982a; Redei, 1982); but seldom in situ. A similar protocol to the barley assay is used principally to detect chlorophyll-deficient mutants in wheat, rice, oats, pea, and tomato (Nilan, 1978).
Much more experience in the in situ monitoring of pesticides is available with the waxy specific locus system in corn (Plewa, 1985). The assay is based on the detection of mutations in the `waxy' character of pollen grains. In brief, the starch of pollen grains having the dominant wild-type allele Wx consists of a mixture of amylose and amylopectine, and it stains bluish-black with iodine. Mutation from dominant to recessive (wx) allele leads to the loss of amylose, and the pollen grain stains red. Since over 106 pollen grains per treatment group can be scored by a rather simple technique in a short time, this genetic analysis has a statistical power comparable to that obtained in the microbial mutagenesis assays. In the in situ experiments, Plewa et al. (1984) evaluated the genotoxic activity of pesticides in field plots (2 x 0.5 m or 10 x 3 m) situated randomly within the corn field. Insecticides and herbicides were applied in their field grade formulation at doses similar to that recommended for the control of pests and weed (Grant et al., 1981; Plewa, 1985). The waxy system is not specific to corn only, and similar assays have been explored in barley and other species (Nilan et al., 1981).
Mutations in haploid pollen grains can be explored for the estimation of induced changes in the gene Adh+ coding for alcohol dehydrogenase. Grains of corn having Adh- mutations stain yellow, whereas Adh+ stains blue (Schwartz, 1981).
Another group of specific locus mutation assays in plants, used occasionally to test the genotoxicity of pesticides, is based on specially constructed tester strains, or clones, that are heterozygotic in one or two loci. This enables the manifestation of somatic mutations shortly after the application of a test compound. Somatic mutations are expressed as sectors of differently coloured tissues on leaves (soybean, tobacco, clover, corn) or on flower petals and stamen hairs (Tradescantia). The stamen hair assay in Tradescantia interspecific hybrids is one of the most sensitive laboratory tests; it has also been used for in situ monitoring of gaseous air pollutants, giving the results 23 weeks after the exposure of flower buds (Schairer et al., 1981). The test has been explored also for fumigants (e.g., 1,2-dibromoethane) and pesticides in liquid form (e.g., maleic hydrazide) (Gichner et al., 1982; Veleminsky and Gichner, 1988). The tobacco assay, based on the detection of green and white sectors on yellow-green leaves, seems to be very suitable for testing pesticides (e.g., maleic hydrazide) in the soil (Briza et al., 1984). This assay, as well as the soybean assay (Vig, 1975), detects not only reversion or forward mutations, but also somatic recombinations. A tester strain of perennial white clover, with the leaf-colour marker gene, could be a good indicator for long-term monitoring in situ (Nilan, 1978), but has never been used for this purpose.
14.3.3 DETECTION OF GENOTOXIC METABOLITES FORMED IN PLANTS FROM PESTICIDES
Formation of mutagenic metabolites from xenobiotics is a well-known phenomenon in animals (Bartsch et al., 1982). Such a mechanism was not considered in plants until it was found to occur in corn sprayed with atrazine and in barley treated with sodium azide. Stable metabolites were isolated, and they caused mutations in microbial tester strains (Plewa and Gentile, 1976; Owais and Kleinhofs, 1988). These observations stimulated research to find suitable and efficient methods to detect mutagenic metabolites in plants formed from environmental compounds including pesticides. Recently, the state of the art in this field has been summarized by Plewa et al. (1988).
There are at least three ways to detect the metabolic activation of pesticides into mutagenic products in plants (Gentile et al., 1986; Veleminsky and Gichner, 1988):
1.
Exposure of plants or plant-cell cultures to pesticides and testing for mutagenic activity of plant extracts in any mutagenicity assay like Salmonella, yeast, or human and rodent cell assay. If extracts from pesticide-treated plants increase the mutagenicity and extracts from unexposed plants are non-mutagenic, the plant genotoxic product can be further purified and characterized. For atrazine's mutagenic metabolite in corn, this can be done by centrifugal fractionation, gel permeation on Sephadex, and HPCL chromatography (Means et al., 1988), whereas for azidoalanin (a mutagenic product of sodium azide in barley), purification and identification are performed by other procedures (Owais and Kleinhofs, 1988).
2.
Preparation of extracts from untreated plants that retain enzyme activities and their co-incubation with pesticides of interest and with an indicator organism (e.g., bacteria, yeasts, or animals cells). The activation of the pesticide to the mutagenic product mediated by plant enzymes is scored according to the frequency of mutations in the indicator organism. This system has been used successfully by numerous laboratories for pesticide studies to detect the formation of mutagenic metabolites from captan, diquat, maleic hydrazide, triallate, and ziram (Rasquinha et al., 1988).
3.
Co-incubation of cultured plant cells (instead of plant extract) with the pesticide and with the indicator strain for mutagenicity. This system overcomes many differences associated with the preparation of plant extracts and maintenance of their enzymatic activity (Plewa et al., 1988).
14.4 CONCLUSIONS
This chapter deals mostly with the biological assays that are, or might be, used for detection of toxic, principally genotoxic, effects of pesticides in plants. Compared to chemical and biochemical methods, these assays are simple, inexpensive, less laborious, and able to detect toxicity without the researcher's knowing or understanding the steps that produce the ultimate effect(s). This observation does not imply that chemical and biochemical methods are less important or less used than bioassays. Attempts have been made to detect metabolites that may be formed, and residues and impurities that may remain or that may accumulate in plants used either as human food or as animal feed and forage. In general, experimental strategies and chemical or biochemical methods of extraction, clean-up, and quantitative and qualitative determinations are the same for plants as for animals. Radioactively labelled pesticides, combined with thin-layer and high-performance liquid chromatography or gas chromatogaphy have contributed substantially to great progress in the residue and metabolite analysis in plants (Klein and Scheunert, 1982; Lord, 1982; Shimabukuro et al., 1978; Mumma and Davidonis, 1983; Lamoureux and Rusness, 1986).
Crops and wild plants are some of the most frequent recipients of pesticides among biota. Different species and forms (varieties, cultivars) respond differently to different pesticides in terms of their uptake, translocation, degradation or activation, and accumulation of residues and metabolites, the consequence of which is differential toxicity, including genotoxicity. Nevertheless, such data on plants are generally not taken into account in the assessment of the environmental hazard of pesticides (Hardy, 1982; Costa et al., 1987).
---------- FOLLOW-UP ----------
QUESTION: so what would be a good pesticides that i could get cheep and test but, see the affects easily and write a report on for the science fair we're having?..... thanks so much for responding to my first question it was really helpful.... ^^
ANSWER: Hi there. To see the fastest results I would get a couple non selective weed killers,such as Round Up(glyophosate). Check your local home and garden center. If you do this be sure to follow safety instructions and get your parents to help with it.Hope this helps. Bill
---------- FOLLOW-UP ----------
QUESTION: Dear Bill,
Thank you so much for the artical but, where did you get it from? I need to know where you got it from so I can write a MLA bibliography card for it for my class on Tuesday.
-shira
AnswerHi there. Here is the http address and a reference list. Just copy what you need. Let me know what grade WE GET on the report. lol Good luck,Bill
http://www.icsu-scope.org/downloadpubs/scope49/chapter14.html
14.5 REFERENCES
Banki, L. (1978) Bioassay of Pesticides in the Laboratory, Akademiai Kiado, Budapest.
Bartsch, H., Kuroki, T., Roberfroid, M. and Malaveille, C. (1982) Metabolic activation systems in vitro for carcinogen/mutagen screening tests. In: DeSerres, F. J. and Hollaender, A. (Eds) Chemical Mutagens, Plenum Press, New York, London, pp. 95-161.
Briza, J., Gichner, T. and Veleminsky, J. (1984) Somatic mutations in tobacco plants after chronic exposure to maleic hydrazide and its diethanolamine and potassium salts. Mutat. Res. 139, 25-28.
Brown, T. (1992) Chapter 15 in this volume.
Campbell, T. A., Gentner, W. A. and Danielson, L. L. (1981) Evaluation of herbicide interactions using linear regression modeling. Weed Sci 29, 378-381.
Cartwright, P. M. (1976) General growth responses of plants. In: Audus, L. J. (Ed.) Herbicides, Physiology, Biochemistry, Ecology, Vol. 1, Academic Press, London, New York, San Francisco, pp. 55-82.
Chancellor, R. J. (1979) The long-term effects of herbicides on weed populations. Ann. Appl. Biol. 91, 125-146.
Cole, D. J. (1983) The effects of environmental factors on the metabolism of herbicides in plants. Aspects Appl. Biol. 4, 245-252.
Cole, H., Mackenzie, D., Smith, C. B. and Bergman, E. L. (1968) Influence of various persistent chlorinated insecticides on the macro and micro element constituents of Zea mays and Phaseolus vulgaris growing in soil containing various amounts of these materials. Bull. Environ. Contam. Toxicol. 3, 141-153.
Constantin, M. J. (1982) Plant genetic systems with potential for the detection of atmospheric mutagens. In: Tice, R. R., Costa, D. L. and Schaich, K. M. (Eds) Genotoxic Effects of Airborne Agents, Plenum Press, New York, London, pp. 159-177.
Costa, L. G., Galli, C. L. and Murphy, S. D. (Eds) (1987) Toxicology of Pesticides: Experimental, Clinical and Regulatory Perspectives, NATO ASI Series Vol. H 13, Springer-Verlag, Berlin, Heidelberg, 320pp.
Crosby, D. G. (1982) Pesticides as environmental mutagens. In: Fleck, R. A. and Hollaender, A. (Eds) Genetic Toxicology: An Agricultural Perspective, Plenum Press, New York, London, pp. 201-218.
Evans, G. C. (1972) The Quantitative Analysis of Plant Growth, Blackwell Scientific Studies in Ecology, University of California Press, Berkeley, 734pp.
Frans, R., Corbin, B., Johnson, D. and McClelland, M. (1988) Herbicide Field Evaluation Trials on Field Crops, 1987, Arkansas Agricultural Experiment Station Res. Series Report No. 365, University of Arkansas, Little Rock, 80pp.
Gentile, S. M., Gentile, G. J. and Plewa, M. J. (1986) In vitro activation of chemicals by plants: a comparison of techniques. Mutat. Res. 164, 53-58.
Gichner, T., Veleminsky, J. and Pokorny, V. (1982) Somatic mutations induced by maleic hydrazide and its potassium and diethanolamine salts in the Tradescantia mutation assay. Mutat. Res. 103, 289-293.
Grant, W. F. (1972) Pesticides subtle promoters of evolution. IV Symposium Biol. Hung. 12, 43-50. Hungarian Academy of Sciences, Budapest.
Grant, W. F. (1982a) Cytogenetic studies of agricultural chemicals in plants. In: Fleck, R. A. and Hollaender, E. (Eds) Genetic Toxicology. An Agricultural Perspective, Plenum Press, New York, London, pp. 353-378.
Grant, W. F. (1982b) Chromosome aberrations assays in Allium. Mutat. Res. 99, 273-291.
Grant, W. F., Zinoveva-Stahevitch, A. E. and Zura, K. D. (1981) Plant genetic test systems for the detection of chemical mutagens. In: Stich, H. F. and San, R. H. C. (Eds) Short-Term Tests for Chemical Carcinogens, Springer-Verlag, New York, Heidelberg, Berlin, pp. 200-216.
Grant, W. F. and Zura, K. D. (1982) Plants as sensitive in situ detectors of atmospheric mutagens. In: Heddle, J. A. (Ed.) Mutagenicity: New Horizons in Genetic Toxicology, Academic Press, New York, pp. 407-434.
Gressel, J. (1987) In vitro plant cultures for herbicide prescreening. In: LeBaron, H. M., Mumma, R. O., Honeycutt, R. C. and Duesing, J. H. (Eds) Biotechnology in Agricultural Chemistry, American Chemistry Society, Washington DC, pp. 41-52.
Hance, R. J. and McKone, C. E. (1976) The determination of herbicides. In: Audus, L. J. (Ed.) Herbicides, Physiology, Biochemistry, Ecology. Vol. 2, Academic Press, London, New York, San Francisco, pp. 393-446.
Hardy, A. R. (1982) Ecotoxicology of pesticides: the laboratory and field evaluation of the environmental hazard presented by new pesticides. In: Costa, L. G., Galli, C. L. and Murphy, S. D. (Eds) Toxicology of Pesticides: Experimental, Clinical and Regulatory Perspectives, NATO ASI Series Vol. H 13, Springer-Verlag, Berlin, Heidelberg, pp. 185-196.
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