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World Scientists' Statement: Calling for a Moratorium on GM
(Genetically Modified) Foods and Crops

<<http://www.twnside.org.sg/souths/twn/bio.htm>

Third World Network / TWN update:
[Last Modified: 7. Apr 1999]
<<http://www.twnside.org.sg/souths/twn/title/world-cn.htm>

World Scientists' Statement --

Calling for a Moratorium on GM Crops and Ban on Patents

We the undersigned scientists call upon our Governments to:

Impose an immediate moratorium on further environmental releases of
transgenic crops, food and animal-feed products for at least 5 years.

Ban patents on living organisms, cell lines and genes.

Support a comprehensive, independent public enquiry into the future of
agriculture and food security for all, taking account of the full range of
scientific findings as well as socioeconomic and ethical implications.

1. We are extremely concerned over the continued release and
commercialization of transgenic crops, food and animal-feed products in the
face of growing scientific evidence of hazards to biodiversitv, food
safety, human and animal health, while neither the need nor the benefits of
genetic engineering agriculture are yet proven.

1.1 New scientific evidence have convinced us of the need for an immediate
moratorium on releases.

1.1.1. Herbicide resistant transgenes have spread to wild relatives by
cross-pollination in both oilseed rape and sugar beet,1 creating many
species of potential superweeds. One study shows that transgenes may be up
to 30 times more likely to escape than the plant's own genes2

1.1.2. Bt-toxins engineered into a wide range of transgenic plants already
released into the environment may build up in the soil and have devastating
impacts on pollinators and other beneficial insects3

1.1.3. Serious doubts over the safety of transgenic foods are raised by
new revelations on the results of animal feeding experiments. Potatoes
engineered with snowdrop lectin fed to rats caused highly significant
reduction in weight of many organs, impairment of immunological
responsiveness and signs suggestive of viral infection.4

1.1.4. Research from the Netherlands show that antibiotic resistant marker
genes from genetically engineered bacteria can be transferred horizontally
to indigenous bacteria at a substantial frequency of 10-7 in an artificial
gut5

1.1.5. Researchers in the US found widespread horizontal transfer of a
yeast genetic parasite to the mitochondrial genome of higher plants6,
raising serious concerns over the uncontrollable horizontal spread of
transgenes and marker genes from transgenic plants released into the
environment.

2. The patenting of living organisms, cell lines and genes under the Trade
Related Intellectual Property Rights agreement are sanctioning acts of
piracy of intellectual and genetic resources from Third World nations7, and
at the same time, increasing corporate monopoly on food production and
distribution. Small farmers all over the world are being marginalized,
threatening long term food security for all8.

3. The Governments of industrialized nations, by voting for patents on
organisms, cell lines and genes, including human genes, are in danger of
allowing corporations unrestricted exploitation of their citizens and
natural resources through the treaties being negotiated in the WTO and
other fora Environmental standards, food safety standards and even basic
human rights will be sacrificed to corporate financial imperatives9.

4. Governmental advisory committees lack sufficient representation from
independent scientists not linked to the industry. The result is that an
untried, inadequately researched technology has been rushed prematurely to
the market, while existing scientific evidence of hazards are being
downplayed, ignored, and even suppressed10, and little independent research
on risks are being carried out.

5. The technology is driven by an outmoded, genetic determinist science
that supposes organisms are determined simply by constant, unchanging genes
that can be arbitrarily manipulated to serve our needs; whereas scientific
findings accumulated over the past twenty years have invalidated every
assumption of genetic determinism11. The new genetics is compelling us to
an ecological, holistic perspective, especially where genes are concerned.
The genes are not constant and unchanging, but fluid and dynamic,
responding to the physiology of the organism and the external environment,
and require a stable, balanced ecology to maintain stability.

Endnotes:

1. Brookes, M. (1998). Running wild, New Scientist 31 October; Snow, A. and
Jorgensen, R. (1998). Costs of transgenic glufosinate resistance
introgressed from Brassica napus into weedly Brassica rapa. Abstract,
Ecologicil Society of America, Baltimore, Aug. 6, 1998.

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

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

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

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

6. Cho, Y., Qui, 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.

7. See Shiva, V. (1998). Biopiracy: The Plunder of Nature and Knowledge,
Green Books, London; also Latin American Declaration on Transgenic
Organisms, Quito, 22 Jan. 1999.

8. The Corner House (1998), Food? Health? Hope? Genetic Engineering and
World Hunger, Briefing 10.

9. See Mander, J. and Goldsmith, E. eds. (1996). The Case against the
Global Economy and for a Turn toward the Local, Sierra Club Books, San
Francisco.

10. See note 4.

11. See Ho, M. W. (1998, 1999). Genetic Engineering Dream or Nightmare? The
Brave New World of Bad Science and Big Business, Gateways Books and Third
World Network, Bath and Penang.

==============
Subject: World Scientists' Statement[2]: Supplementary Information on the

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 technology 25 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 rape 34 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 k|nstlicher Herbizidresistenz: Verbessert sich
die R|ckstandssituation? Verfahren zurTechnikfolgenabschatzung des Anbaus
von Kulturpflanzen mit gentechnisch erzeugter Herbizidresistenz. van den
Daele W. P|hler 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"
<<http://www.btinternet.com/%7Enlpwessex>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., Kdmmer,
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.


Scientists involved in the launch of the Statement:

1. Prof. Arpad Pusztai, Biochemical Immunologist, formerly Rowett
Institute, UK
2. Dr. Susan Bardocz, Geneticist, Rowett Institute, UK
3. Prof. Joe Cummins, Geneticist, University of Western Ontario, Canada
4. Prof. Martha Crouch, Biologist, Indiana University, USA
5. Prof. Terje Traavik, Virologist, University of Tromso, Norway
6. Prof. Brian Goodwin, Biologist, Schumacher College, UK
7. Prof. Martha R. Herbert, Pediatric Neurology, Massachusetts Gen.
Hospital, USA
8. Dr. Mae-Wan Ho, Geneticist and Biophysicist, Open University, UK 9. Dr.
Vyvyan Howard, Toxipathologist, Liverpool University, UK 10. Dr. Vandana
Shiva, Research Institute for Science and Ecology, India 11. Prof. Peter
Saunders, Biomathematician, King's College, London, UK 12. Dr. Christine
von Weisaeker, Ecoropa, Germany 13. Dr. Tewolde Egziabher, Agronomist,
Environmental Protection Authority, Ethiopia
14. Prof. Phil Bereano, Engineering, University of Washington, USA

Contact: Mae-Wan Ho/Angela Ryan, Institute of Science in Society
Tel/Fax: 44-181-441-6480
E-mail:i-sis@Dircon.co.uk


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