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World Scientists' Statement
Supplementary Information on the Hazards of Genetic Engineering Biotechnology

1. Genetic engineering is a new departure from conventional breeding and introduces significant differences.

1.1. Conventional breeding involves crossing related species, and plants with the desired characteristics are selected from among the progeny for reproducing, and the selection is repeated over many generations. Genetic engineering bypasses reproduction altogether. It transfers genes horizontally from one individual to another (as opposed to vertically, from parent to offspring), often making use of infectious agents as vectors or carriers of genes so that genes can be transferred between distant species that would never interbreed in nature. For example, human genes are transferred into pig, sheep, fish and bacteria. Toad genes are transferred into tomatoes. Completely new, exotic genes, are being introduced into food crops.

1.2. Natural infectious agents exist which can transfer genes horizontally between individuals. These are viruses and other pieces of parasitic genetic material, called plasmids and transposons, which are able to get into cells and then make use of the cell's resources to multiply many copies of themselves or to jump into (as well as out of ) the cell's genome. While the natural agents are limited by species barriers, genetic engineers make artificial vectors by combining parts of the most infectious natural agents, and design them to overcome species barriers, so the same vector may now transfer, say, human genes, which are spliced into the vector, into the cells of all other mammals, or cells of plants. Once inside the cell, the artificial vector carrying the foreign gene(s) can then insert into the cell's genome, and give rise to a genetically engineered organism.

1.3. Typically, foreign genes are introduced with strong genetic signals - called promoters or enhancers, most often from viruses - to boost the expression of the genes to well above the normal level that most of the cell's own genes are expressed. Such viral promoters are used even in cases of so-called "vectorless" transfers, where gene expression "cassettes" are introduced by injection, biolistic bombardment and other physical means. 1 There will also be selectable "marker genes" introduced along with the gene(s) of interest, so that those cells that have successfully integrated the foreign genes into their genome can be selected. The most commonly used marker genes are antibiotic resistant genes, which enable the cells to be selected with antibiotics. These marker genes often remain in the genetically engineered organisms.

2. Genetic engineering introduces new dangers and problems to health and biodiversity.

There are four main sources of hazards and problems: those due to the new genes and gene products introduced; unintended effects inherent to the technology; interactions between foreign genes and host genes; and those arising from the spread of the introduced genes by ordinary cross-pollination as well as by horizontal gene transfer.

3. Hazards may come from new genes and gene products.

New genes and gene products are introduced into our food, often from bacteria and viruses and other non-food species that we have never eaten before, and certainly not in the quantities produced in the genetically engineered crops, where they are typically expressed at high levels. The long term impacts of these genes and gene products on human health will be impossible to predict, particularly as the products are not segregated and there is no post-market monitoring.

3.1. Bt-toxins may have major impacts on biodiversity.

There is evidence that one class of gene products most commonly introduced, the bt-toxins, from the soil bacterium, Bacillus thuringiensis, targetted against insect pests, are harmful to beneficial species such as bees.² That is because they are introduced in a truncated, preactivated, non-selective form. Harmful effects can even go up the food-chain. Lacewings fed on pests that have eaten genetically engineered bt-maize took longer to develop and were two to three times more likely to die.³ Purified bt-toxins, similar to ones found in some lines of transgenic bt-crops, do not disappear when added to soil but instead become rapidly bound to clay and humic acid soil particles. The bound bt-toxins, unlike free toxins, are not degraded by soil microbes, nor do they lose their capacity to kill soil insects.⁴ Unlike suspensions of the bacteria which have been used as sprays by organic farmers, in which the toxins are inactivated by uv light, the engineered toxins are released directly into the soil, thereby escaping degradation.The buildup of bt-toxins in the soil will have devastating impacts on pollinators and other beneficial insects. At the same time, it will accelerate the evolution of bt-resistance among pest, rendering the toxin ineffective as a pesticide. Bt-resistance is already a major problem only years after the first release, and scientists are recommending 20 to 40% of non-transgenic crop to be simultaneously planted as "refugia" to slow down the evolution of resistance.⁵

3.2. Transgenic snow-drop lectin is harmful to beneficial insects.

Yet another transgenic plant has been shown to harm beneficial insects up the food-chain. Ladybirds fed on aphids that have eaten transgenic potato with snow-drop lectin lived half as long, laid 38% fewer eggs that were 4 times more likely to be unfertilized and 3 times less likely to hatch.⁶ This transgenic potato has now been revealed to be highly toxic to rats (see below), and is most probably harmful to small mammals in the wild.

3.3 Hazards arise from transgenic plants engineered to be resistant to broad-spectrum herbicides.

By far the major category of transgenic plants are engineered to be resistant to broad-spectrum herbicides such as glyphosate.

3.3.1. The toxicity of glyphosate is well-documented.⁷ Acute toxicity of some glyphosate products include eye and skin irritation, cardiac depression and vomiting. In California, glyphosate is found to be the third most commonly-reported cause of pesticide-related illness among agricultural workers. The toxicities are often associated with supposedly inert solvents and detergents in some formulations which greatly increase the harmful effects of glyphosate. These synergistic interactions are now widely recognized.⁸ Chronic toxicity of glyphosate include testicular cancer, reduced sperm counts and other negative reproductive impacts in rats.⁹ There are also indications that at least some glyphosate formulations cause mutations in genes.¹⁰

3.3.2. Broad-spectrum herbicides will have major impacts on biodiversity.¹¹ They kill all other plants indiscriminately. This will destroy wild plants as well as insects, birds, mammals and other animals that depend on the plants for food and shelter. In addition, Roundup (Monsanto's formulation of glyphosate) can be highly toxic to fish. Glyphosate also harms earthworms and many beneficial mycorrhizal fungi and other microorganisms that are involved in nutrient recycling in the soil. It is so generally toxic that researchers are even investigating its potential as an antimicrobial.¹²

3.3.3. Herbicide resistant transgenic plants may lead to increased use of herbicides, contrary to what is being claimed. The transgenic plants themselves are already turning up as volunteer plants after the harvest, and have to be controlled by additional sprays of other herbicides.¹³ The use of glyphosate with genetically engineered resistant plants will encourage the evolution of glyphosate resistance in weeds and other species, even without cross-pollination. A ryegrass highly resistant to glyphosate has already been found in Australia.¹⁴ Resistance evolves extremely rapidly because all cells have the capability of mutating their genes at high rates to resistance if they are exposed continuously to sub-lethal levels of toxic substances including herbicides, pesticides and antibiotics. This is inherent to the "fluidity" of genes and genomes that has been documented within the past 20 years.¹⁵ It will render resistant plants useless after several generations, as the herbicide is widely applied. At the same time, resistant weeds and pathogens may become increasingly abundant. Additional herbicides will then have to be used to control the resistant weeds.

3.3.4 Herbicide resistant transgenic crops are incompatible with sustainable agriculture. Many studies within the past 10 to 15 years have shown that sustainable organic agriculture can improve yields and regenerate agricultural land degraded by the intensive agriculture of the green revolution.¹⁶ Sustainable organic agriculture depends on maintaining natural soil fertility as well as on mixed cropping and crop rotation. This has been reversing the destructive effects of intensive agriculture that have led to falling productivity since that 1980s. Glyphosate resistant plants requires application of glyphosate which not only kills other species of plants but harms mycorrhizal fungi symbiotically associated with the roots of plants, which are now found to be crucial for maintaining both species diversity and productivity of ecosystems.¹⁷ The depletion of mycorrhizal fungi in intensive agriculture could therefore decrease both plant biodiversity and ecosystem productivity, while increasing ecosystem instability. "The present reduction in biodiversity on Earth and its potential threat to ecosystem stability and sustainability can only be reversed or stopped if whole ecosystems, including ecosystem components other than plants are protected and conserved."¹⁸

4. Problems due to unintended effects inherent to the technology.

Genetic engineering organisms is hit or miss, and not at all precise, contrary to misleading accounts intended for the public, as it depends on the random insertion of the artificial vector carrying the foreign genes into the genome. This random insertion is well-known to have many unexpected and unintended effects including cancer, in the case of mammalian cells. ¹⁹ Furthermore, the effects can spread very far into the host genome from the site of insertion.²⁰

4.1. This is attested to by the high failure rates in making transgenic animals, and gross deformities among the "successes",²¹ which are unacceptable in terms of animal welfare.

4.2. There have also been many failures among crops that have been commercialized and widely planted.²² The Flavr Savr tomato was a commercial disaster and has disappeared. Monsanto's bt-cotton failed to perform in the field in both US and Australia in 1996, and suffered excessive damages from bt-resistant pests. Monsanto's 1997 Roundup resistant cotton crops fared no better. The cotton balls drop off when sprayed with Roundup and farmers in seven states in the US have sought compensation for losses. The transgenic "Innovator" herbicide tolerant canola failed to perform consistently in Canada. This has led the Saskachewan Canola Growers Association to call for an official seed vigor test.

4.3. There is widespread instability of transgenic lines, they generally do not breed true.²³ One of the main problems is gene silencing - cellular processes that prevent foreign genes from being expressed.²⁴ The instability of transgenic lines are inherent to the hit or miss technology, untried technology²⁵ which may ruin our agricultural base and severely compromise world food security.

5. Unexpected and unintended effects will also arise from interactions between foreign genes and genes of the host organism.

No gene functions in isolation. Among the unintended effects relevant to food safety are new toxins and allergens, or changes in concentrations of existing toxins and allergens.

5.1. In 1989, a genetically engineered batch of tryptophan killed 37 and made 1500 ill, some seriously to this day, the suspected culprit was a trace contaminant which may have arisen from the genetic engineering.²⁶

5.2. A Brazil nut allergen was identified in soya bean genetically engineered with a brazil nut gene.²⁷

5.3. Soya beans are known to have at least 16 proteins that can cause allergic reactions, which differ for different ethnic groups. A major allergen, trypsin-inhibitor which also has antinutritional effects, was found to be 26.7% higher in Monsanto's transgenic soya beans approved for market on the basis of "substantial equivalence",²⁸ and hence safe for human consumption.²⁹ The same transgenic soya reduced growth rate of male rats and increased milk fat in cows.³⁰ It is also suspected that the transgenic soya may have higher levels of phytoestrogens linked to reproductive abnormalities in mice, rats and ewes as well as humans.³¹ Women with oestrogen-induced breast cancer, pregnant women and children may be particularly susceptible to phytoestrogens.³²

5.4. Serious doubts have been raised over the safety of transgenic foods by recent revelations on the results of animal feeding experiments. Potatoes engineered with snowdrop lectin fed to rats caused highly significant reduction in both dry and wet weights of many essential organs: intestine, liver, spleen, thymus, pancreas and brain. In addition, it resulted in impairment of immunological responsiveness and signs suggestive of viral infection.³³ The two transgenic lines were substantially different from each other and from the unengineered (unmodified) parent with respect to potato-lectin content, protease inhibitor, gross composition and amino acid content, yet the official audit concludes that they were "substantially equivalent".

6. Hazards arise from the uncontrollable spread of transgenes and antibiotic resistance marker genes.

Genetic pollution, as opposed to chemical pollution cannot be recalled. Genes, once released, have the potential to multiply and recombine out of control.

6.1. Transgenes and marker genes have spread to wild relatives by cross-pollination, creating superweeds.

This has occurred in oilseed rape³⁴ and sugar beet,³⁵ creating potential superweeds. Spread of genes by cross-pollination is to be expected, whether the plants are transgenic or not. However, a recent report suggests that transgenes may be up to 30 times more likely to escape than the plant's own genes.³⁶ This raises the question as to whether other mechanisms for the spread of the transgenes (and marker genes) are present in transgenic plants, the most obvious being horizontal gene transfer to unrelated species.

6.2. Transgenes and marker genes may also spread by horizontal gene transfer.

The same cellular mechanisms that enable the artificial vector carrying the foreign genes to insert into the genome can also mobilize the vector to jump out again to reinsert at another site or to infect other cells. For example, the enzyme, integrase, which catalyzes the integration of viral DNA into the host genome, also functions as a disintegrase catalyzing the reverse reaction. These integrases belong to a superfamily of similar enzymes present in all genomes from viruses and bacteria to higher organisms.³⁷

6.2.1 Secondary horizontal tranfer of transgenes and antibiotic resistant marker genes from genetically engineered crop plants into soil bacteria and fungi have been documented in the laboratory.³⁸ Despite the misleading title in one of the publications,³⁹ a high "optimal" gene transfer frequency of 6.2 x 10-2 was found in the laboratory, from which the authors "calculated" a frequency of 2.0 x 10-17 under extrapolated "natural conditions". The natural conditions, are of course, largely unknown.

6.2.2 Plants engineered with genes from viruses to resist virus attack actually showed increased propensity to generate new, often super-infectious viruses by horizontal gene transfer and recombination with infecting viruses.⁴⁰

6.2.3 A genetic parasite belonging to yeast, a group I intron, was found to have jumped into many unrelated species of higher plants recently.⁴¹ Until 1995, this parasite was thought to be largely confined to yeast and only one genus of higher plants out of the 25 surveyed had the parasite. But in a new survey of species from 335 genera of higher plants, 48 were found to have the parasite. These 48 genera were in five different families: Asterids, Rosids, Monocots, Piperales, and Magnoliales. Sequence analyses indicate that the same group I intron is present in all the higher plants and that almost all of them represent independent horizontal gene transfer events. The researchers themselves raise serious concerns about releasing transgenic crops into the environment, given that horizontal gene transfer is now found to be so widespread.

6.2.4. Thus, genetically engineered crops, many of which still carry antibiotic resistant marker genes may spread these genes to pathogenic bacteria in the environment, as there is now evidence that DNA released from dead and live cells are not readily broken down, but are rapidly adsorbed onto clay, sand and humic acid particles where they retain the ability to infect (transform) other organisms. They may also contribute to generating new viral pathogens. This is particularly relevant in the light of the current world health crisis in drug and antibiotic resistant infectious diseases, and evidence indicating that horizontal gene transfer has been responsible for spreading drug and antibiotic resistance genes as well as creating new pathogens.⁴²

6.2.5. There is also evidence that DNA is not broken down rapidly in the gut as previously supposed. Thus, transgenes and antibiotic resistance marker genes may spread to bacteria in the gut.⁴³ New research from the Netherlands show that antibiotic resistant marker genes from genetically engineered bacteria can be transferred to indigenous bacteria at a substantial frequency of 10-7 in an artificial gut.⁴⁴

6.2.6. Viral DNA fed to mice has been found to resist digestion in the gut. Large fragments passed into the bloodstream and into white blood cells, spleen and liver cells. In some instances, the viral DNA may integrate into the mouse cell genome.⁴⁵ Viral DNA is now known to be more infectious than the intact virus, which has a protein coat wrapped around the DNA. For example, intact human polyoma virus injected into rabbits had no effect, whereas, injection of the naked viral DNA gave a full-blown infection.⁴⁶ Many kinds of artificially constructed vectors are found to infect mammalian cells.⁴⁷ Thus, the foreign DNA introduced by artificial vectors into genetically engineered plants and animals may constitute a health hazard by itself. As mentioned above, integration of foreign DNA into cells are well-known to have many adverse effects including cancer.

7. Existing scientific evidence indicates that genetic engineering agriculture is an dangerous diversion.

Genetic engineering agriculture not only obstructs the implementation of real solutions to the problems of food security for all, but also poses unprecedented risks to health and biodiversity. Far from feeding the world, it will intensify corporate control on food production and distribution which created poverty and hunger in the first place. It will also reinforce existing social structures and intensive agricultural practices that have led to widespread environmental destruction and falling yields since the 1980s.⁴⁸

Endnotes:

1. See Reiss, M.J. and Straughan, R. (1996). Improving Nature? The Science and Ethics of Genetic Engineering, Cambridge University Press, Cambridge

2. See Ho, M.W., Meyer, H. and Cummins, J. (1998). The biotechnology bubble. The Ecologist 28(3), 146-153, and references therein.

3. Hilbeck, A., Baumgartner, M., Fried, P.M. and Bigler, F. (1997). Effects of transgenic Bacillus thuringiensis-corn-fed prey on mortality and development time of immature Chrysoperla carnea (Neuroptera: Chrysopidae). Environmental Entomology

4. Crecchio, C. and Stotzky, G. (1998). Insecticidal activity and biodegradation of the toxin from Bacillus thuringiensis subsp. kurstaki bound to humic acids from soil," Soil Biology and Biochemistry 30, 463-70, and references therein.

5. See Union of Concerned Scientists Newsletter Fall-Winter, 31 Jan. 1999; also, Griffiths, M. (1998). Nature fights back as technology tries to outsmart it. Farming News, October 23, 1998.

6. Birch, A.N.E., Geoghegan, I.I., Majerus, M.E.N., Hackett, C. and Allen, J. (1997). Interaction between plant resistance genes, pest aphid-population and beneficial aphid predators. Soft Fruit and Pernial Crops. October, 68-79.

7. Cox, C. (1995). Glyphosate, Part 2: Human exposure and ecological effects. Journal of Pesticide Reform 15 (4).

8. Howard, V. (1998). Synergistic effects of chemical mixtures. Can we rely on traditional toxicology: The Ecologist 27(4) 193-5.

9. FAO/WHO (1986) Pesticide residues in food. Evaluations Part I and Part II, Rome 29.09 - 8. 10, 1985; Ohnesorge, F.K. (1994). Toxikologische Aspekte. In Nutzpflanzen mit künstlicher Herbizidresistenz: Verbessert sich die Rückstandssituation? Verfahren zurTechnikfolgenabschatzung des Anbaus von Kulturpflanzen mit gentechnisch erzerugter Herbizidresistenz. van den Daele W. Pühler A, Sukopp H (Hrsg.) WZB Berlin.

10. Kale, P.G., Petty, B.T. Jr., Walker, S., Ford, J.B., Dehkordi, N., Tarasia, S., Tasie, B.O., Kale, R. and Sohni, Y.R. (1995). Mutagenicity testing of nine herbicides and pesticides currently used in agriculture. Environ Mol Mutagen 25, 148-53

11. See Greenpeace Report, 1998, and references therein.

12. Roberts, F., Roberts, C.W., Johson, J.J., Kyle, D.E., Drell, T., Coggins, J.R., Coombs, G.H., Milhous, W.K., Tzipori, S., Ferguson, D.J.P., Chakrabarti, D. and McLeod, R. (1998). Evidence for the shikimate pathway in apicomplexan parasites. Nature 393, 801-5.

13. See "Disappointing Biotech Crops" <www.btinternet.com/~nlpwessex>.

14. New Scientist, 6 July, 1996.

15. See Dover, G.A. and Flavell, R.B. (1982). Genome Evolution, Academic Press; also Ho, M.W. 1998, 1999. Genetic Engineering Dream or Nightmare? The Brave New World of Bad Science and Big Busness, Gateways Books and Third World Network, Bath and Penang.

16. See Pretty, J. (1995). Regenerating Agriculture: Policies and Practice for Sustainability and Self-Reliance, Earthscan, London; also Ho (1998,1999), note 11.

17. van der Heijden, M.G.A., Klironomos, J.N., Ursic, M., Moutoglis, P., Streitwolf-Engel, R., Boller, T., Wiemken, A. and Sanders I.R. (1998). Mycorrhizal fungal diversity determines plant variability and productiviy. Nature 396, 69-72.

18. van der Heijden, et al, 1998, p.71. (note 14).

19. Walden, R., Hayashi, H. and Schell, J. (1991). T-DNA as a gene tag. The Plant Journal 1, 281-288; Wahl, G.M., de Saint Vincent, B.R. & DeRose, M.L. (1984). Effect of chromosomal position on amplification of transfected genes in animal cells. Nature 307: 516-520; see also entries in Kendrew, J., ed. (1995). The Encyclopedia of Molecular Biology, Blackwell Science, Oxford; See also note 1.

20. Recently reviewed by Doerfler, W., Schubbert, R., Heller, H., Kämmer, C., Hilger-Eversheim, D., Knoblauch, M. and Remus, R. (1997). Integration of foreign DNA and its consequences in mammalian systems. Tibtech 15, 297-301.

21. See Ho et al, 1998 (note 2) and references therein.

22. See Ho et al, 1998 (note 2) and references therein.

23. See Ho, M.W. and Steinbrecher, R. (1998). Fatal Flaws in Food Safety Assessment: Critique of The Joint FAO/WHO Biotechnology and Food Safety Report, Environmental and Nutritional Interactions 2, 51-84; and references therein.

24. Finnegan H. & McELroy (1994). Transgene inactivation plants fight back! Bio/Techology 12: 883-888.

25. See Ho et al, 1998 (note 2).

26. Mayeno, A.N. and Gleich, G.J. (1994). Eosinophilia-myalgia syndrome and tryptophan production: a cautionary tale. Tibtech 12, 346-352.

27. Nordlee, J.A., Taylor, S.L., Townsend, JA., Thomas, L.A. & Bush, R.K. (1996). Identification of a brazil-nut allergen in transgenic soybeans. The
New England Journal of Medicine March 14, 688-728.

28. Padgette, S.R., Taylor, N.B., Nida, D.L., Bailey, M.R., MacDonald, J., Holden, L.R., and Fuchs R.L. (1996). The composition of glyphosate-tolerant soybean seeds is equivalent to that of conventional soybeans. Journal of Nutrition 126, 702-16.

29. See Ho, M.W. and Steinbrecher, R. (1998). Fatal Flaws in Food Safety Assessment: Critique of The Joint FAO/WHO Biotechnology and Food Safety Report, Environmental and Nutritional Interactions 2, 51-84.

30. Hammond, B.G., Vicini, J.L. Hartnell, G.F., Naylor, M.W., Knight, C.D., Robinson, E.H., Fuchs, R.L. and Padgette, S.R. (1996). The feeding value of soybeans fed to rats, chickens, catfish and dairy cattle is not altered by genetic incorporation of glyphosate tolerance. Journal of Nutrition 1126(3) 717-26.

31. See Oekoinstitut Freiburg: Reply to the Statement made by the Bundesministerium fur Gesundheit (Ministry of Health of the German Federal Republic) on 5 December 1996, in respect of the importation of genetically engineered glyphosate-tolerant soybeans from the company Monsanto, 1997.

32. Dibb, S. (1995). Swimming in a sea of oestrogens - chemical hormone disrupter. The Ecologist 25, 27-31.

33. Leake, C. and Fraser, L. (1999). Scientst in Frankenstein food alert is proved right. UK Mail on Sunday, 31 Jan.; Goodwin, B.C. (1999). Report on SOAEFD Flesible Fund Project RO818, Jan. 23, 1999.

34. See Ho, M.W. and Tappeser, B. (1997). Potential contributions of horizontal gene transfer to the transboundary movement of living modified organisms resulting from modern biotechnology. Proceedings of Workshop on Transboundary Movement of Living Modified Organisms resulting from Modern biotechnology: Issues and Opportunities for Policy-makers (K.J. Mulongoy, ed.), pp. 171-193, International Academy of the Environment, Geneva.

35. Brookes, M. (1998). Running wild, New Scientist 31 October.

36. Bergelson, J., Purrington,c.B. and Wichmann, G. (1998). Promiscuity in transgenic plants. Nature 395, 25.

37. Asante-Appiah E. and Skalka, A.M. (1997). Molecular mechanisms in retrovirus DNA integration. Antiviral Research 36, 139-56.

38. Hoffman, T., Golz, C. & Schieder, O. (1994). Foreign DNA sequences are received by a wild-type strain of Aspergillus niger after co-culture with transgenic higher plants. Current Genetics 27: 70-76; Schluter, K., Futterer, J. & Potrykus, I. (1995). Horizontal gene-transfer from a transgenic potato line to a bacterial pathogen (Erwinia-chrysanthem) occurs, if at all, at an extremely low-frequency. Bio/Techology 13: 1094-1098; Gebhard, F. and Smalla, K. (1998). Transformation of Acinetobacter sp. strain BD413 by transgenic sugar beet DNA. Appl. Environ. Microbiol. 64, 1550-4.

39. Schlutter et al, 1995 (see note 38).

40. Vaden V.S. and Melcher, U. (1990). Recombination sites in cauliflower mosaic virus DNAs: implications for mechanisms of recombination. Virology 177, 717-26; Lommel, S.A. and Xiong, Z. (1991). Recombination of a functional red clover necrotic mosaic virus by recombination rescue of the cell-to-cell movement gene expressed in a transgenic plant. J. Cell Biochem. 15A, 151; Greene, A.E. and Allison, R.F. (1994). Recombination between viral RNA and transgenic plant transcripts. Science 263, 1423-5; Wintermantel, W.M. and Schoelz, J.E. (1996). Isolation of recombinant viruses between cauliflower mosaic virus and a viral gene in transgenic plants under conditions of moderate selection pressure. Virology 223, 156-64.

41. Cho, Y., Qiu, Y.-L., Kuhlman, P. and Palmer, J.D. (1998). Explosive invasion of plant mitochondria by a group I intron. Proc. Natl. Acad. Sci. USA 95, 14244-9; Gray, M.W. (1998). Mass migration of a group I intron: Promiscuity on a grand scale. Proc. Natl. Acad. Sci. USA 95, 14003-5.

42. See Ho, M.W., Traavik, T., Olsvik, R., Tappeser, B., Howard, V., von Weizsacker, C. and McGavin, G. (1998). Gene Technology and Gene Ecology of Infectious Diseases. Microbial Ecology in Health and Disease 10, 33-59.

43. See Ho et al, 1998 (note 42) and refs therein.

44. MacKenzie, D. (1999). Gut reaction. New Scientist 30 Jan., p.4.

45. Schubbert, R., Lettmann, C. & Doerfler, W. (1994). Ingested foreign (phage M13) DNA survives transiently in the gastrointestinal tract and enters the bloodstream of mice. Mol. Gen. Genet. 242: 495-504; Schubbert, R., Renz, D., Schmitz, B. and Doerfler, W. (1997). Foreign (M13) DNA ingested by mice reaches peripheral leukocytes, spleen and liver via the intestinal wall mucosa and can be covalently linked to mouse DNA. Proc. Natl. Acad. Sci. USA 94, 961-6.

46. See Traavik, T. (1995). Too Early May Be Too Late. Ecological Risks Associated with the Use of Naked DNA as a Biological Tool for Research, Production and Therapy (Norwegian), Report for the Directorate for Nature Research Tungasletta 2, 7005 Trondheim. English translation, 1999; Ho et al,
1998 (see note 41); also Ho, 1999 Chapter 10 (see note 17).

47. See Ho et al, 1998 (see note 42); also Ho, 1999 Chapter 10 (see note 11).

48. See Brown, L. R. (1998). Struggling to raise cropland productivity. In State of the World 1998 (L.R. Brown, C. Flavin and H. French, eds.) pp. 79-95, Worldwatch Institute Report, Earthscan Publications, London; Ho, 1999, (note 11), Chapter 9; GeneWatch (1998). Genetically Engineered Food: The Case for a Moratorium.

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