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Murashige, Laura m Pt. 4 PICOUNat.
From: Courtney Bruch [usmaui @hotmail.com]
Sent: Tuesday, December 06, 2011 12:00 PM
To: counciltestimony @co.hawaii.hi.us
Cc: cohmayor @co.hawaii.hi.us; dyagong @co.hawaii.hi.us; dikeda @co.hawaii.hi.us;
jyoshimoto @co.hawaii.hi.us; donishi @co.hawaii.hi.us; fblas @co.hawaii.hi.us;
bsmart @co.hawaii.hi.us; bford @co.hawaii.hi.us; apilago @co.hawaii.hi.us;
phoffman@co.hawaii.hi.us
Subject: Communication 480—Adoption of 2012 HSAC legislative package— labeling of GMOs
Attachments: Testimony letter 2 to the council members.pdf; PROF.pdf; Sensible regulations for GM food
crops- Prof David Schubert.pdf; Weighing the GMO arguments-against.pdf; Revolving
door.jpg
Item: Communication 480—Adoption of 2012 HSAC legislative package— labeling of GMOs
Date: December 7th, 2011
By: Courtney Bruch (Ph:808-283-6837)
Esteemed Council Members of Hawaii/Big Island,
Please find attached my written testimony in support of the GMO labeling bill. cc)
I Strongly support the labeling of GMOs.
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Thank you for your consideration, a �'
Courtney Bruch T
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of4 Ramoda Anand visits Mayor Arakawa!
Dec.6, 2011
Dear Council Members-
Thank you for your willingness to educate yourselves about the multitude of
concerns surrounding genetically engineered organisms. I realize there is plen-
ty of contradicting information. I realize that you all are wanting to make the
best choices for HI and protect the lives of your families and ohana. I also real-
ize that Hawaii has a plantation agricultural heritage that may have provided
jobs but has also been environmentally toxic due to the high use of chemicals.
Because of plantation based agriculture it has become a commonly accepted
practice (to some)to use mass amounts of chemicals for mono crops. GE meth-
ods follow the same system.Without appropriate education,farm workers
(where English is often a second language) are susceptible to being exposed to
harmful chemicals and are not aware of the potential hazards of what they are
cultivating. Many people in the world would prefer to gain profit at the expense
of others health. Monsanto is one of those companies. Only a little research into
this corporation's history will clearly identify this fact. Please watch the docu-
mentary The World According to Monsanto.
I realize our residents need jobs. Multi national companies like Monsanto, Dow,
Syngenta, etc. provide some.There is a certain point in one's life where integrity -
and the health of this planet must come before profit.This is that time!There
are many creative,financially sustainable, ecological job opportunities avail-
able. Let's set our intentions on that mission and set this example for the world.
Let's lead the way!
Concerning GMO's....You can't claim ignorance any more.The beauty of this
HSAC process is that all council members are being educated about this serious
issue. I have spent close to a year dedicated to this HSAC item.
My friend Ramoda Anand, wrote this reso with the help of his aide and intro-
duced it through beloved Maui Council Woman Elle Cochran. Ramoda has
cerebral palsy. He is unable to read or write. His accomplishments with the
assistance of his aides are notable.We care deeply about preserving the integ-
rity of organic and heirloom seeds, supporting health through local, organic
food,as well as making sure that everyone has a RIGHT TO KNOW about GMO
and what they are eating. Ramoda has taught me to be patient and not to be
to hard on Council members who did not support this Res. He told me a story
about how he rebelled when his parents (holistic health practitioners) told him
about the dangers related to gmo foods. Eventually upon more personal study
he changed his mind and is now a champion of GMO Labeling! He is an inspira-
tion to our community and the world!
I will reiterate the message I gave to Maui Council Members in my testimony,
due to this process,YOU are fortunate to know for yourselves and your fami-
lies the health concerns related to GMO's.You have a choice because you have
been informed. Everyone deserves this choice. I invite you to be champions of
healthy,organic food for yourself,your keiki and your island!You're worth it!
We're still learning most economical, least burdensome way to label gmo's.
Please help us in this process.The first thing is to let Hawaii State Legislature
know all counties support gmo labeling by supporting this item in HSAC. Kaua'i
and Maui Counties have already supported it! Mahalo! I expect the same of
Oahu and Hawai'i.
Once this gets to the State Leg.we can modify the Bill so that it is completely
feasible.
It's a win/win/win! Everyone will be able to make a choice, everyone will know
gmo's exist.GMO farmers can take pride in their products they claim are the
same and or exemplary.We will be able to identify and track this new food
technology in the case of health concerns that may be related.This is really a
'no brainer.:)
Please look over the scientific evidence in the attachments I have provided!
Mahalo for your time! Here's to your health! Support the Labeling of GMO's.
Sincerely,
Courtney Bruch,
L.M.T., B.F.A
Haiku, HI
Upcountry Sustainability
GMO FREE MAUI
Kipahulu Community Association
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pr
•
Norfolk Genetic Information Network
24 July 2002
PROF. SCHUBERT ON THE RISKS OF GM FOOD
fwd by Dr Robt Mann to the Ban-GEF list
***
The Risks of GM Food
Professor David Schubert
Cellular Neurobiology Lab, Salk Institute for Biological Studies, San
Diego, USA
July 2002 ..
As a cell biologist I am very much discouraged by the content of the
ongoing debate about introducing genetically modified (GM) plants into
the marketplace. While the voiced concerns usually center around
irrational emotional arguments on the one hand, and the erroneous
concept that genetic engineering is just like plant breeding on the other, I
believe that the three issues which should be of most concern on the
basis of established science receive little or no discussion.
These are:
1. that introducing the same gene into 2 different types of cells can
produce two very distinct protein molecules;
2. the recent observations that the introduction of any gene, be it from a
different or the same species, always significantly changes overall gene
expression and therefore the phenotype of the recipient cell; and
3. the possibility that enzymatic pathways introduced to synthesize small
molecules such as vitamins can interact with endogenous pathways to
produce novel molecules.
The potential consequence of all of these perturbations could be the
production of biomolecules that are either toxic or carcinogenic, and
there is no _a priori_ way of predicting the outcome.
I will give a few examples and then argue why GM food is not a safe
alternative.
In addition to their primary sequence of amino acids, the structure and
biological activity of proteins can be modified by the addition of
molecules such as phosphate, sulfate, sugars or lipids. The nature of
these secondary modifications is totally dependent upon the cell type in
which they are expressed. For example, if a protein involved in the
cause of Alzheimer's disease, the beta amyloid precursor protein, is
expressed in liver cells it contains covalently-attached chondroitin
sulfate carbohydrate, while the identical gene expressed in brain nerve
cells contains a much simpler sugar. This is because each cell type
expresses a unique repertoire of enzymes capable of modifying proteins
after they are synthesized. Once modified, the biological activity of the
molecule may be changed. In the case of the beta-amyloid precursor
protein, the adhesive properties of the cells are changed, but there is, at
our current state of knowledge, no way of knowing the biological
effects of these modifications.
The second concern is the potential for inducing the synthesis of
poisonous or toxic compounds following the introduction of a foreign
gene. These observations are clearly at odds with the individuals who
imply that everything is fine because they are simply introducing one
gene. In fact, the introduction of a single gene invariably alters the gene
expression pattern of the whole cell and each cell of the individual or
plant responds differently. One recently published example is the
transfection of a receptor gene into human cells. In this case, the gene
was a closely related isoform of an endogenously expressed gene. The
pattern of gene expression was monitored using gene chip technology,
and the mRNA levels of 5% of the genes was significantly upregulated
or downregulated. Similarly, the simple introduction of a bacterial
enzyme used for growth selection of transfected cells changes the
expression of 3% of the genes. While these types of unpredicted
changes in gene expression are very real, they have not received much
attention outside the community of the DNA chip users.
Furthermore, they are not unexpected. The maintenance of a specific
cell phenotype is a very precise balancing act of gene regulation, and
any perturbation is going to change the overall patterns of gene
expression.
The problem, like that of secondary modifications, is that there is
currently no way to predict the resultant changes in protein synthesis.
Third, the introduction of genes for a new enzymatic pathway into plants
could lead to the synthesis of totally novel or unexpected products via
the interaction with endogenous pathways. Some of the products could
be toxic. For example, retinoic acid (vitamin A) and derivatives of
retinoic acid are used in many signaling events that control mammalian
development. Since these compounds are soluble and work at ultralow
concentrations, a GM plant making vitamin A may also produce retinoic
acid derivatives which act as agonists or antagonists in these pathways,
resulting in abnormal embryonic development.
1
Given the fact that genetically modified plants are going to make
proteins in different amounts and perhaps totally new proteins than their
parental species, what are the potential outcomes? A worst case scenario
could be that an introduced bacterial toxin is modified to make it toxic to
humans. Direct toxicity may be rapidly detected once the product enters
the marketplace, but carcinogenic activity or toxicity caused by
interaction with other foods would take decades to detect, if ever. The
same outcomes would be predicted for the production of toxins or
carcinogens via indirect changes in gene expression.
Finally, if the above problems are real, what can be done to address
these concerns? The issue of secondary modification could be
addressed by continual monitoring of the introduced gene product by
mass spectroscopy.
The problem is that some secondary modifications, like phosphorylation
or sulfation can be lost during purification. However, the best, and to me
the only reasonable solution, is to require all genetically engineered
plant products for human consumption be tested for toxicity and
carcinogenicity before they are marketed. These safety criteria are
required for many chemicals and all drugs, and the magnitude of harm
caused by a widely consumed toxic food would be much greater than
that of any single drug.
Professor David Schubert
Cellular Neurobiology Lab
The Salk Institute for Biological Studies
P.O. Box 85800
San Diego, CA 92186-5800
USA
Phone: (001) (858) 453-4100
Email: schubert@salk.edu
http://www.gmwatchiorg/latest-listing/1-news-items/
9243-sensible-regulations-for-gm-food-crops-prof-david-
schubert-1272005
Sensible regulations for GM food crops - Prof David
Schubert
Tuesday, 12 July 2005 13:20
This is an unedited version of the article by David Schubert, a Professor in the
Cellular Neurobiology Laboratory at The Salk Institute, published as 'Regulatory
Regimes for Transgenic Crops' in the journal Nature Biotechnology (23, 785 -
787; July 2005)
http://www.nature.com/nbt/journal/v23/n7/full/nbt0705-785b.html
Schubert is responding to Bradford et al's, 'Regulating transgenic crops sensibly:
lessons from plant breeding, biotechnology and genomics' which was published
in Nature Biotechnology in April 2005 (23(4):439-44).
http://www.nature.com/nbt/journal/v23/n4/abs/nbt1084.html
After analysing their arguments, Schubert concludes, "Because of the high
mutagenicity of the transformation procedures used in GE, the
assumptions made by Bradford et al. and also the FDA about the precision
and specificity of plant GE are incorrect. Nonetheless, it appears that the
positions of Bradford et al. and the biotech industry, as well as the current
regulatory framework [in the U.S.] for the labeling and safety testing of GE food
crops, is to maintain the status quo and hope for the best.
"The problem is that there are no mandatory safety testing requirements
for unintended effects and that it may take many years before any
symptoms of a GE-caused disease appear. In the absence of strong
epidemiology or clinical trials, any health problem associated with an
illness caused by a GE food is going to be very difficult, if not impossible,
to detect unless it is a disease that is unique or normally very rare."
SENSIBLE REGULATIONS FOR GE FOOD CROPS
By David Schubert
In a recent article Bradford and colleagues argued that the methods used to
produce food crops should not be the focus of regulatory oversight, only the
phenotypic traits of the resultant plants as defined in terms of standard
agricultural practice1. They propose that any risk and safety assessments of
crops produced by genetic engineering (GE) should be based only upon the
nature of the introduced genes. They also claim that transgenic crops face a
"daunting" array of regulatory requirements.
However, safety testing requirements in the United States are largely voluntary
and in my view inadequate. These regulations have been reviewed elsewhere2
and will not be discussed further. Safety concerns related to the GE process itself
as well as its unintended consequences are set aside by Bradford et al as
irrelevant, for they claim that the products of genetic events that occur naturally
and with standard plant breeding techniques are fundamentally the same as
those that occur with GE. Are these arguments a valid reflection of what is known
about the precision and consequences of the GE process as compared with
naturally occurring genomic variation?
The basic assumption underlying the concept of a one-to-one relationship
between the transgene and the resultant phenotype is that the GE process is
relatively precise. However, none of the current transgene insertion techniques
permit control over the location of the insertion site or the number and orientation
of the genes inserted. Indeed, over one-third of all Agrobacterium-mediated
insertion events disrupt functional DNA3,4. These and related transformation and
cell culture-induced changes in chromosomal structure have been recently
documented in great detail5. For example, translocations of up to 40 Kb6,
scrambling of transgene and genomic DNA7, large scale deletions of over a
dozen genes8 and frequent random insertions of plasmid DNA9 can all be
caused by the procedures used to make GE plants. In fact, the most commonly
used transformation procedure is sometimes itself used as a mutagen10, and
can activate dormant retrotransposons that are highly mutagenic1l. Moreover,
mutations linked to the transgene insertion site cannot be removed by additional
breeding as long as there is selection for the transgene itself. Collectively these
data indicate that the GE process itself is highly mutagenic.
Some modern breeding technologies introduce new traits into plants via chemical
or radiation mutagenesis or by wide cross hybridizations that overcome natural
species barriers. Mutagenesis was used in the United States during the middle
part of the last century, but food crops made by this technique now constitute
less than a few percent of US production, with sunflowers being the major
representative12. However, plants produced by wide crosses, such as those
between quackgrass and bread wheat to yield a widely planted grain that has all
of the chromosomes of wheat and an extra half genome of the quackgrass, while
unique, are fundamentally different from those produced by either mutagenesis
or GE. In wide crosses and other forms of ploidy manipulation there are clearly
changes in gene dosage, and proteins unique to only one parent can be
produced in the hybrid, but there is no a priori reason to assume that mutations
are going to occur simply because there is a change in chromosome or gene
number. While the extent and suddenness of all of these modern breeding
technologies are unlike anything known to occur during the course of evolution or
with traditional breeding, only GE and mutagenesis introduce large numbers of
mutations. Any new cultivars derived by the latter two methods should be
subjected to similar regulatory requirements.
Bradford et al. correctly state that plants normally contain the same
Agrobacterium and viral DNA sequences that are used to create GE transfection
constructs, but fail to point out that with GE these pieces of DNA are part of a
cassette of genes for drug resistance along with strong constitutive viral
promoters that are used to express foreign proteins at high levels in all parts of
the plant, hardly a natural event. They incorrectly imply that changes in ploidy,
gene copy number, recombination, and high genomic densities of transposable
elements in normal plants continually lead to mutations and changes in gene
expression similar to those caused by GE.
Ploidy is notoriously unstable in plants, but changes involve moving around large
blocks of intact genes while maintaining their regulated expression pattern. It
should also be remembered that recombination is not the same as random
mutagenesis, for there has been tremendous selective pressure for alleles to
express functionally similar proteins. The statement that "retrotransposons
continuously insert themselves between genes" is incorrect, for these high copy
number elements are transpositionally inactive in normal modern food plantsl3,
have evolved and rearranged in the distant pastl4, but can be activated by tissue
culture or by mutagenesisl l. In fact their discovery by Barbara McClintock was
facilitated by the use of mutagenized corn13.
While Bradford et al. propose that regulatory efforts should be focused upon the
expression of the transgene, I believe that the major hazards of the highly
mutagenic plant transformation techniques are the potentials for a decrease in
nutritional content or an increase in dangerous metabolites. While it is widely
recognized that the breeding of some crops can produce varieties with harmful
characteristics, millennia of experience have identified these crops, and breeders
test new cultivars for known harmful compounds, such as alkaloids in
potatoes15,16. In contrast, unintended consequences arising from the random
and extensive mutagenesis caused by GE techniques opens far wider
possibilities of producing novel, toxic, or mutagenic compounds in all sorts of
crops. Unlike animals, plants accumulate thousands of nonessential small
molecules that provide adaptive benefits under conditions of environmental or
predator-based stressl7. Estimates are that they can make between 90,000 and
200,000 phytochemicals with up to 5000 in one speciesl8. These compounds
are frequently made by enzymes with low substrate specificityl9 in which
mutations can readily alter substrate preference20,21
There are many examples of unpredictable alterations in small molecule
metabolism in GE organisms. In yeast genetically engineered to increase
glucose metabolism, the GE event caused the unintended accumulation of a
highly toxic and mutagenic 2-oxoaldehyde called methylglyoxal22. In a study of
just 88 metabolites in four lines of potatoes transformed for altered sucrose
metabolism, Roessner et al. found that the amounts of the majority of these
metabolites were significantly altered relative to controlsl8. In addition, nine of
the metabolites in GE potatoes were not detected in conventional potatoes.
Given the enormous pool of plant metabolites, the observation that 10% of those
assayed are new in one set of transfections strongly suggests that undesirable or
harmful metabolites may be produced and accumulate23. Contrary to the
suggestions of Bradford et al., Kuiper and his colleagues strongly recommend
that each transformation event should be assayed for these types of unintended
events by metabolic profiling24.
A well documented horticultural example of unintended effects is the alteration in
the shikimic acid pathway in Bt corn hybrids derived from Monsanto's MON810
and Syngenta's Btl1 plants as well as glyphosate-tolerant soybeans. Stem tissue
of both groups of plants has elevated levels of lignin, an abundant non-digestible
woody component that makes the plants less nutritious for animal feed25,26.
Components of this same biochemical pathway also produce both flavonoids and
isoflavonoids that have a high nutritional value, and rotenone, a plant-produced
insecticide that may cause Parkinson's disease27. Isoflavonoids are abundant in
legumes like soy beans, and rotenone is synthesized directly from isoflavones in
many legume species28. Because of the promiscuity of many plant enzymes and
the large and varied substrate pools of phytochemical intermediates, it is
impossible to predict the products of enzymes or regulatory genes mutated
during the GE event23. While I are not aware of any testing of GE soybeans for
rotenone, it has been shown that glyphosate-tolerant soybeans sprayed with
glyphosate have a reduced flavonoid content29.
The safety testing of GE crops need not be as extensive as that done with drugs,
food additives or cosmetics. Many suggestions have been put forward (see, for
example 30,2,5,24) including those by the World Health Organization3l. I believe
that the most important safety tests include metabolic profiling to detect
unexpected changes in small molecule metabolism24 and the Ames test to
detect mutagens32. Molecular analysis of the gene insertion sites and
transformation-induced mutations5 should also be performed along with both
multigenerational feeding trials in rodents to assay for teratogenic effects and
developmental problems, and allergenicity testing performed according to a
single rigorous protocol3l The animal studies are of particular importance for
crops engineered to produce precursors to highly biologically active compounds
such as Vitamin A and retinoic acid, molecules that can act as teratogens at high
doses33.
In summary, Bradford et al. state that there is a low risk from the consumption of
GE plants "where no novel biochemical or enzymatic functions are imparted".
The question is, of course, how can one know if a novel and potentially harmful
molecule has been created unless the testing has been done? How can one
predict the risk in the absence of an assay? Because of the high mutagenicity of
the transformation procedures used in GE, the assumptions made by Bradford et
al. and also the FDA 34 about the precision and specificity of plant GE are
incorrect. Nonetheless, it appears that the positions of Bradford et al. and the
biotech industry, as well as the current regulatory framework for the labeling and
safety testing of GE food crops, is to maintain the status quo and hope for the
best.
The problem is that there are no mandatory safety testing requirements for
unintended effects2 and that it may take many years before any symptoms of a
GE-caused disease appear. In the absence of strong epidemiology or clinical
trials, any health problem associated with an illness caused by a GE food is
going to be very difficult, if not impossible, to detect unless it is a disease that is
unique or normally very rare. Therefore, while GE may be able to enhance world
health and food crop production , its full potential is likely to remain unfulfilled
until rigorous pre-release safety testing can provide some assurance to
consumers that the products of this new technology are safe to eat.
REFERENCES:
1. Bradford, K. J., Van Deynze, A., Gutterson, N., Parrott, W. & Strauss, S. H.
Regulating transgenic crops sensibly: lessons from plant breeding, biotechnology
and genomics. Nat Biotechnol 23, 439-44 (2005).
2. Freese, W. & Schubert, D. Safety testing of genetically engineered food. 21
Biotechnology and Genetic Engineering Reviews, 299-325 (2004).
3. Szabados, L. et al. Distribution of 1000 sequenced T-DNA tags in the
Arabidopsis genome. Plant J 32, 233-42 (2002).
4. Forsbach, A., Schubert, D., Lechtenberg, B., Gils, M. & Schmidt, R. A
comprehensive characterization of single-copy T-DNA insertions in the
Arabidopsis thaliana genome. Plant Mol Biol 52, 161-76 (2003).
5. Wilson, A., Latham, J. & Steinbrecher, R. 35 (EcoNexus, Brighton, UK, 2004).
6. Tax, F. E. & Vernon, D. M. T-DNA-associated duplication/translocations in
Arabidopsis. Implications for mutant analysis and functional genomics. Plant
Physiol 126, 1527-38 (2001).
7. Makarevitch, I., Svitashev, S. K. & Somers, D. A. Complete sequence analysis
of transgene loci from plants transformed via microprojectile bombardment. Plant
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Mol Biol 52, 421-32 (2003).
8. Kaya, H. et al. Hosoba toge toge, a syndrome caused by a large chromosomal
deletion associated with a T-DNA insertion in Arabidopsis. Plant Cell Physiol 41,
1055-66 (2000).
9. Kim, S. R. et al. Transgene structures in T-DNA-inserted rice plants. Plant Mol
Biol 52, 761-73 (2003).
10. Weigel, D. et al. Activation tagging in Arabidopsis. Plant Physiol 122, 1003-13
(2000).
11. Hirochika, H., Sugimoto, K., Otsuki, Y., Tsugawa, H. & Kanda, M.
Retrotransposons of rice involved in mutations induced by tissue culture. Proc
Natl Acad Sci U S A 93, 7783-8 (1996).
12. Ahloowalia, B. S., Maluszynski, M. & Nichterlein, K. Global impact of
mutation-derived varieties. Euphytica 135, 187-204 (2004).
13. Feschotte, C., Jiang, N. & Wessler, S. R. Plant transposable elements: where
genetics meets genomics. Nat Rev Genet 3, 329-41 (2002).
14. Brunner, S., Fengler, K., Morgante, M., Tingey, S. & Rafalski, A. Evolution of
DNA Sequence Nonhomologies among Maize lnbreds. Plant Cell 17, 343-60
(2005).
15. Korpan, Y. I. et al. Potato glycoalkaloids: true safety or false sense of
security? Trends Biotechnol 22, 147-51 (2004).
16. Ewen, S. W. & Pusztai, A. Effect of diets containing genetically modified
potatoes expressing Galanthus nivalis lectin on rat small intestine. Lancet 354,
1353-4 (1999).
17. Verpoorte, R. in Metabolic Engineering of Plant Secondary Metabolism (eds.
Verpoorte, R. &Alfermann, A. W.) 1-29 (Kluwer Academic Publishers, Dordrecht ,
The Netherlands, 2000).
18. Roessner, U. et al. Metabolic profiling allows comprehensive phenotyping of
genetically or environmentally modified plant systems. Plant Cell 13, 11-29
(2001).
19. Schwab, W. Metabolome diversity: too few genes, too many metabolites?
Phytochemistry 62, 837-49 (2003).
20. Zubieta, C. et al. Structural basis for substrate recognition in the salicylic acid
carboxyl methyltransferase family. Plant Cell 15, 1704-16 (2003).
21. Johnson, E. T. et al. Alteration of a single amino acid changes the substrate
specificity of dihydroflavonol 4-reductase. Plant J 25, 325-33 (2001).
22. (nose, T. & Murata, K. Enhanced accumulation of toxic compound in yeast
cells having high glycolytic activity: A case study on the safety of genetically
engineered yeast. Intl J Food Sci Tech 30, 141-6 (1995).
23. Grotewold, E. Plant metabolic diversity: a regulatory perspective. Trends
Plant Sci 10, 57-62 (2005).
24. Kuiper, H. A., Kleter, G. A., Noteborn, H. P. & Kok, E. J. Assessment of the
food safety issues related to genetically modified foods. Plant J 27, 503-28
(2001).
25. Saxena, D. & Stotzky, G. Bt corn has a higher lignin content than non-Bt
corn. Amer J Botany 88, 1704-6 (2001).
26. Gertz, J. M., Vencill, W. K. & Hill, N. S. in Proceedings of the 1999 Brighton
Crop Protection Conference: Weeds 835-840 (British Crop Protection Council,
Farnham, UK, 1999).
27. Betarbet, R. et al. Chronic systemic pesticide exposure reproduces features
of Parkinson's disease. Nature Neurosci. 3, 1301-1306 (2000).
28. Morgan, E. D. & Wilson, I. D. in Comprehensive Natural Products Chemistry
(ed. Mori, K.) 363-375 (Pergamon Press/Elsevier Science, Oxford, 1999).
29. Lappe, M. A., Bailey, E. B., Childress, C. & Setchell, K. D. R. Alterations in
clinically important phytoestrogens in genetically modified, herbicide-tolerant
soybeans. J Med Foods 1, 241-245 (1999).
30. Edmonds_Institute. Manual for assessing ecological and human health
effects of genetically engineered organisms. http://www.edmonds-institute.org/
manual.html. (Edmonds Institute, 1998).
31. FAO-WHO. Evaluation of Allergenicity of genetically modified foods. Report of
a Joint FAO/WHO expert consultation on allergenicity of foods derived from
biotechnology. January 22-25, 2001. http://www.fao.org/es/ESN/food/pd/
allergygm.pdf. (2001).
32. Maron, D. M. &Ames, B. N. Revised methods for the Salmonella
mutagenicity test. Mutat Res 113, 173-215 (1983).
33. McCaffery, P. J., Adams, J., Maden, M. & Rosa-Molinar, E. Too much of a
good thing: retinoic acid as an endogenous regulator of neural differentiation and
exogenous teratogen. Eur J Neurosci 18, 457-72 (2003).
34. Kessler, D. A., Taylor, M. R., Maryanski, J. H., Flamm, E. L. & Kahl, L. S. The
safety of foods developed by biotechnology. Science 256, 1747-9, 1832 (1992).
FOOD AND AGRICULTURE ORGANIZATION OF THE UNITED NATIONS
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FAO NEWSROOM
http://www.fao.org/english/newsroom/focus/2003/gmo8.htm
Weighing the GMO arguments: against
The main arguments that have been put forward against the
use of GMOs in agriculture include:
Potential negative effects on the environment
• Genes can end up in unexpected places: Through "gene escape"
they can pass on to other members of the same species and perhaps
other species. Genes introduced in GMOs are no exception, and
interactions might occur at gene, cell, plant and ecosystem level.
Problems could result if, for example, herbicide-resistance genes got
into weeds. So far, research on this is inconclusive, with scientists
divided - often bitterly. But there is scientific consensus that once
widely released, recalling transgenes or foreign DNA sequences,
whose safety is still subject to scientific debate, will not be feasible.
• Genes can mutate with harmful effect: It is not yet known
whether artificial insertion of genes could destabilize an organism,
encouraging mutations, or whether the inserted gene itself will keep
stable in the plant over generations. There is no conclusive data on
this issue.
• "Sleeper" genes could be accidentally switched on and active
genes could become "silent": Organisms contain genes that are
activated under certain conditions -- for example, under attack from
pathogens or severe weather. When a new gene is inserted, a
"promoter" gene is also inserted to switch it on. This could activate a
"sleeper" gene in inappropriate circumstances. This is especially
relevant in long-lived organisms - such as trees. Sometimes the
expression of genes is even "silenced" as a result of unknown
interactions with the inserted gene.
• Interaction with wild and native populations: GMOs could
compete or breed with wild species. Farmed fish, in particular, may
do this. GM crops could pose a threat to crop biodiversity, especially
if grown in areas that are centres of origin of that crop. In addition,
GM crops could compete with and substitute traditional farmers'
varieties and wild relatives that have been bred, or evolved, to cope
with local stresses. For example, local varieties in Latin America
permitted the recovery from the catastrophic potato blight in Ireland
in the 1840s. Today such plants often help improve climate tolerance
and disease resistance. If genetically modified crop varieties
substitute them, they could be lost, but the same applies to
improved varieties developed by conventional breeding methods.
• Impact on birds, insects and soil biota: Potential risks to non-
target species, such as birds, pollinators and micro-organisms, is
another important issue. Nobody quite knows the impact of
horizontal flow of GM pollen to bees' gut or of novel gene sequences
in plants to fungi and soil and rumen bacteria. Besides, it is feared
that widespread use of GM crops could lead to the development of
resistance in insect populations exposed to the GM crops. Planting
"refuge" areas with insect-susceptible varieties is advised to reduce
the risk of insect populations evolving resistance due to the
widespread growing of GMO Bt-crops.
Potential negative effects on human health
• Transfer of allergenic genes: These could be accidentally
transferred to other species, causing dangerous reactions in people
with allergies. For example, an allergenic Brazil-nut gene was
transferred into a transgenic soybean variety. Its presence was
discovered during the testing phase, however, and the soybean was
not released.
• Mixing of GM products in the food chain: Unauthorized GM
products have appeared in the food chain. For example, the GM
maize variety Starlink, intended only for animal feed, was
accidentally used in products for human consumption. Although
there was no evidence that Starlink maize was dangerous to
humans, strict processing controls may be required to avoid similar
cases in the future.
• Transfer of antibiotic resistance: Genes that confer antibiotic
resistance are inserted into GMOs as "markers" to indicate that the
process of gene transfer has succeeded. Concerns have been
expressed about the possibility that these "marker genes" could
confer resistance to antibiotics. This approach is now being replaced
with the use of marker genes that avoid medical or environmental
hazards.
Potential socio-economic effects
• Loss of farmers' access to plant material: Biotechnology
research is carried out predominantly by the private sector and there
are concerns about market dominance in the agricultural sector by a
few powerful companies. This could have a negative impact on
small-scale farmers all over the world. Farmers fear that they might
even have to pay for crop varieties bred from genetic material that
originally came from their own fields when they buy seeds from
companies holding patents on specific genetic modification "events".
Some argue that the World Trade Organization's agreement on
Trade-Related Intellectual Property Rights (TRIPS) encourages this,
but there are options to protect farmers' traditional practices within
that agreement. Also, the new International Treaty on Plant Genetic
Resources for Food and Agriculture recognizes the contributions of
farmers to the conservation and use of plant genetic resources over
time and for future generations. It provides for an international
framework to regulate access to plant genetic resources and
establishes a mechanism to share the benefits derived from their
use.
• Intellectual property rights could slow research: The
proprietary nature of biotechnology products and processes may
prevent their access for public-sector research. This might have a
stronger negative impact in developing countries where no private
research initiatives are in place. In addition, most developing
countries still do not provide patent protection to biotechnological
products and technologies. Because patents have a national scope,
the entry of products developed through proprietary biotechnologies
could be prevented in those external markets where patent
protection exists.
• Impact of "terminator" technologies: Although these are still
under development and have not yet been commercialized, they
would, if applied, prevent a crop from being grown the following
year from its own seed. This means that farmers could not save
seeds for planting the next season. Some believe that this
technology, also known as the Technology Protection System, could
have the advantage of preventing out-crossing of GM seeds.
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