Submitted by Dr Helen Fullerton, Farming
and Livestock Concern UK
I am a retired agricultural chemist who now
researches on matters of human and animal health, particularly
nutrition. I have contributed to the consultations on Professor
Philip James's Food Standard Agency proposal and to the White
Paper "A force for Change". Farming and Livestock Concern
UK is a network of farmers and allied interests.
1. THE FSA AND
Genetically modified organisms (GMOs) were not
identified in the White Paper nor in the consultation on draft
Legislation for the Food Standard Agency (FSA), nevertheless it
is now recognised they will be a major concern. I draw attention
to clause 19(2) of the Food Standards Bill: "The Agency
shall take into account of:
(a) the nature and magnitude of any risks
to public health, and or risks, which are relevant to the decision
(including any uncertainty as to the adequacy or reliability of
the available information);
(b) the likely costs and benefits of the
exercise or non-exercise of the power or its exercise in any manner
which the Agency is considering."
Also I draw attention to the Guiding Principles
3"The Agency's decisions should be proportionate
to the risk; pay due regard to costs as well as benefits to those
affected by them and avoid over-regulation."
I put the case that GMOs are an unacceptable
risk because their effects are unpredictable with respect both
to food safety and security of food supply.
2. SUBSTANTIAL EQUIVALENCE
In risk assessment it is only required that
the amounts of known components (usually restricted to nutrients,
toxins and allergens) be the same as that in a comparable non-GMO
foodstuff and devoid of the inserted DNA for it to be declared
"substantially equivalent" with respect to safety, and
it will be approved for marketing by the Advisory Committee on
Novel Foods and Processes (ACNFP). For "fast track approval"
(60 days) the foodstuff must also be devoid of the protein product,
as in the case of soya oil derived from GM-soya [1
paragraph 673]. The EU Commission and the Government propose that
"only products where the transgene or its product are detectable
should be labelled" [2 paragraph 137]. This means
that if either are present below a certain threshold of detectability
(a) would not need to be labelled; and
(b) would be considered substantially equivalent.
At present the detectable limit for GM is 0.1 per cent.
The Lords suggest an agreed EU threshold of
2 per cent [2 paragraph 142]. This may lead to import
disagreements, invoking the WTO: in US and Canada labelling is
only required to identify the presence of potential health or
safety risks and where there are significant changes to the compositional
or nutritional value when compared to non-engineered food [2
Labelling is seen in the EU and UK as necessary
to win consumer confidence and provide consumer choice rather
than as an essential safeguard, enabling identification in case
something goes wrong. Traceability is deemed too difficult and
costly and best left to supermarkets [2 paragraph 117].
It is recommended to be replaced by monitoring.
Monitoring involves both risk assessment and
post-marketing surveillance. ACNFP identifies any injurious protein
product of inserted genes by monitoring, using databases of toxic
and allergic sequences. If one of these is present in the known
protein product e.g., the enzyme conferring resistance to a herbicide
or pest, or if the foodstuff contained higher levels of toxicity
than a comparable non-GM, it would not be given market approval
[1 paragraph 724]. The EU Directive proposes that the
seed company perform the monitoring. The Lords demurred, recommending
that it be done by an independent body, funded by the applicants
[2 paragraph 102].
The value of tests to detect the presence of
transgene DNA is to check whether or not the food or ingredient
has been genetically engineered, e.g., for purposes of labelling.
DNA is detected via polymerase chain reaction (PCR) amplification.
Costs escalate as levels become low as in processed food. Protein
product and metabolite analysis is rarely undertaken, because
antibodies must be raised against the protein and few are available.
[1 Memorandum of the Laboratory of the Government Chemist
Ltd pp. 358-66].
Despite all the cautious measures, the entire
edifice of risk assessment and its dependence on the concept of
substantial equivalence is unsafe. It takes no account of any
risk that might arise from the presence of an unpredictable, unknown
protein or metabolite produced by the genetic manipulation, or
of a changed behaviour of the protein product. Examples follow.
3. THE SNOWDROP
Professor Arpad Pusztai, a leading expert in
lectins (a type of glycoprotein) was concerned that incorporation
of the snowdrop (Galanthus nivalis) gene into potato tubers
might be injurious to health. He believes that experiments are
not being done to find out if the genetic modification induces
unpredictable nutritional effects on the consumers of GM crops.
World wide only one peer-reviewed paper has examined this question
(Pusztai pers.comm). In 1995 the Scottish Office Agriculture,
Environment and Food Department (SOAEFD) commissioned a three
year multicentre project whose main objective was "to
identify genes encoding anti-nutritional factors which will be
suitable for transfer into plants to enhance their resistance
towards insects and nematode pests, but will have minimum impact
on non-target beneficial organisms, the environment, livestock
fed on those plants and which will present no health risks for
humans either directly or indirectly through the food chain."
There is much interest in the snowdrop lectin
(GNA) gene since it is expected its product will be toxic to sucking
insects particularly in rice crops, and to nematodes in root crops,
by interfering with the pests' digestion. When the gene was introduced
into potato tubers the lectin comprised up to a maximum of 0.5
per cent of the total root protein and led to a reduction in nematode
females of 80 per cent.3 These benefits must be set
against the risks. Researchers at the Scottish Crops Research
Institute (SCRI) found its incorporation into the potato leaf
led to lowered fertility and lifespan of the ladybirds feeding
on the aphid larvae.4. Professor Pusztai who co-ordinated
research at the Rowett Research Institute (RRI) found5:
(i) The starch and glucose content of the
transgenic GNA potatoes were different to those of the parent
potatoes, as were the level of potato lectin, and of trypsin and
chymotrysin inhibitors. In one line the raw or baked transenic
contained nearly 20 per cent less protein than its parent. SCRI
scientists had already found a decreased foliar glycoalkaloid
content.6 Pusztai commented: "The results clearly
indicate gene silencing, suppression and or somaclonal variation
as a result of gene insertion . . . the GNA-GM potato lines were
not substantially equivalent to the parent tubers".
(ii) 10-day feeing experiments on rats showed
that digestion and absorption of a transgenic potato-based diets
were retarded in comparison with parent potato diets, and there
was a reduction in weight of most organs. This, together with
a partial liver atrophy on feeding boiled transgenic potato diets
and enlargement of jejunum, pancreas and testes on feeding raw
GNA-GM potato diets suggested a lack of equivalence of the metabolic
consequences between feeding GM and parent potatoes.
(iii) Potatoes spiked with the snowdrop lectin
did not show these abnormalities. The abnormalities were thus
a consequence of the genetic manipulation.
(iv) Lymphocytes from rats given transgenic
potato diets were almost always less responsive to mitogenic stimuli,
indicating immuno-suppression. In contrast, snowdrop lectin-spiked
potato diets in some instances stimulated the immuno-response.
Many plants contain lectins, notably the legumes.
They are in the tomato and widespread in seeds and storage organs
where they may have a protective function against pests but are
benign to the mammal. No doubt when asked for their approval ACNFP
would have consulted their data base to see if the snowdrop lectin
contained a toxic sequence similar to the kidney bean lectin.
If it did not, as indeed the rats fed the GNAspiked potatoes
suggest, would it have been given approval?
After his appearance on World in Action 10 August
98, Professor Pusztai was dismissed from the Rowett 14 August
and forbidden under the terms of the BBSRC staff code (chapters
11, 12) from speaking or publishing in defence of his research.
His report  was suppressed and the embargo only
lifted under media pressure 17 February 1999. The team has been
disbanded and the research quietly discontinued, despite that
many questions remain to be answered. One can only conclude the
project was abandoned under pressure from GMO interests, particularly
Montsanto who have already given £240,000 to the Rowett for
research. If GM companies were required to do pharmacological
toxicity testing as above, it would not only be expensive, but
might give uncomfortable results as in the case of bovine somatotropin
4. THE EFFECTS
It is often claimed there is no scientific evidence
that transgenic crops are not substantially equivalent. There
is little proof because:
(a) it is not looked for; and
(b) if found, the matter is buried in the
literature or else hushed up.
Also hushed up is the nature of GM technology
itself. Pusztai attributed his transgenic results to "gene
silencing and/or somaclonal variation." Nowhere in the House
of Lords Report  is there mention of either, nor
did those giving evidence draw attention to them. The single exception
was the account given by Dr Michael Antoniou on behalf of Greenpeace
[1 Greenpeace memorandum, Appendix 2 pages 36-39].
Since their occurrence is unpredictable and the risks cannot be
quantified, this can be the only reason that the Government's
advisors neglected to inform the Lords about them, except by obliquely
emphasising "it is not the gene that matters, but how it
(i) Gene silencing: When a foreign gene is
inserted into an organism, the DNAlike other tissuescan
recognise self from non-self  and attempts to inactivate
the intruder by silencing or suppressing the gene, usually by
attaching a methyl group to the DNA. The gene will not be expressed
and the looked-for characteristic e.g., insect resistance, cold
tolerance, etc., will not appear, or may fail to appear in the
progeny. More significantly, plant genes with a similar sequence
may also inadvertently be switched off.
(ii) Somaclonal variation: this is the rearrangement
of plant genetic material during tissue culture and plant regeneration
from a single cell . All GM plants are grown from
cells cultured in a dish. Conventional breeders use the same technique,
but without the added complication of the "foreignness"
of the gene. The results are totally unpredictable. Genes do not
work in isolation but in an interdependent network, their expression
determined by the activities of the cell, the reactions of the
organism and environmental influences. The rearrangement may mean
that proteins are expressed in different cells, enzymes work faster
or more slowly, or are switched on at inappropriate times. These
in turn as one may surmise in Pusztai's rats can affect the nutritional
quality of the food, introduce unknown toxins or alter metabolism
5. FURTHER EXAMPLES
(i) A transgenic yeast engineered for an
increased rate of sugar fermentation with multiple copies of one
of its own genes resulted in the accumulation of a metabolite
methyl glyoxal 30 times higher than in the original strains. The
authors pointed out that these levels could be mutagenic and suggested
the concept of substantial equivalence for the safety assessment
of genetically engineered food was not always applicable to genetically
engineered microbes .
(ii) The most famous case is that of a GM
tryptophan genetically engineered in bacteria to produce a cheap
food supplement of this essential amino acid by a Japanese company
Showa Denko. In 1989 in USA 5,000 people became ill with eosnophilia
myalgic syndrome. Thirty-seven died and 1,500 were permanently
disabled. The disaster was eventually traced to the engineered
tryptophan and the presence of a toxin at a concentration of less
than 0.1 per cent of the product. It has never been ascertained
whether the toxin was produced by the genetic manipulation or
in the production process . But we note that:
(a) since the product was not labelled "GMO"
it was indistinguishable from the natural tryptophan on the shelves.
(b) At a concentration of 0.1 per cent it
would today be considered below the threshold limit and classified
as substantially equivalent.
(iii) In a field experiment, the mainly self-pollinating
Arabidosis thuliana had been engineered to be resistant
to the herbicide chlorsulphuron via a mutation in the enzyme acetolactate
synthase. It should have been substantially equivalent to a mutant
wild type expressing the same mutation. The plants are insect-pollinated
and it was found that the wild weed growing along side the test
plants was 20 times more likely to be fertilised by the transgenic
plant than by the mutated one, i.e., it as 20 times more likely
to confer herbicide resistance to the native and create a super
weed . Although not directly relevant to food,
this case is analagous to the differing effects on rats of Pusztai's
GNA-GMO potatoes and GNA-spiked potatoes. In both cases it was
the genetic manipulation that created the changed and unwanted
(iv) We do not know whether the widespread
crop failures in transgenic cotton (see below) were due to gene
silencing and/or to the pressure of a new environment on the GMO.
6. VIRAL HAZARDS
Another matter that is hushed up is the "construct",
aptly described by Professor Mark Williamson as the scaffolding
[1 paragraphs 519-20], necessary to ferry the transgene
into position and provide it with an on-switch (the promoter),
an off-switch (the terminator), and a marker for identifying those
cells that have been modified and will be grown into plants. The
most popular promoter is cauliflower mosaic virus. A major worry
in genetic engineering is that a fragment of viral DNA or RNA
will combine with other fragments or with a benign virus to cause
a virulent disease in crops, beneficial insects, animals or humans.
Given the multiplicity of virus used and the scale, it may be
only a matter of time.
7. FOOD SECURITY
The FSA has no remit for the environmental impact
of GMOs. Nevertheless there is a link here with the security of
food supplies. Bearing in mind that even low probability events
will occur if scale and time increase, foreseeable problems include:
(i) The development of pest resistance. The
most widely used toxin conferring protection to crops is the product
of the Bt gene extracted from Bacillus thuringiensis. Commercial
releases include transgenic maize, potatoes, cotton, tobacco and
leafy vegetable crops. Montsanto's cotton boll-guard Bt-cotton
bred in California lost resistance to bollworm in the droughty
climate of the southern states and had to be sprayed to save it.
Australian farmers were up in arms last year when they too lost
their cotton crop or had to spray it. In the laboratory it was
found that the diamond back-moth, a major pest of cabbages developed
resistance in a few generations against four strains of Bt via
a genetic change in a single gene .
(ii) The destruction of pest predators and
of pollinators. Already ladybirds , lacewings 
and pollinators including our precious bees  have
been shown at risk. Crop yields in recent years have already declined
due to the destruction of pollinators by chemical sprays .
Should there be crop failures around the globe,
due to the scale and uniformity of GM planting it will not be
a matter of unsafe food but of food scarcity.
The FSA should avoid over-regulation and intrusion
into the freedom of the public to choose its own food. Examples
of unwarranted interference include the attempt to restrict the
availability of vitamin B6, the attempt to ban unpasteurised milk
and the imposed ban on beef on the bone. The issue of GMOs is
exactly the opposite. Here we have a hazardous technology foisted
on the public by commercial interests and the desire of government
not to jeopardise UK competitiveness "by any undue delay,
cost or burden [2 paragraph 171] . . . or to impede
scientific progress" [2 paragraph 123]. The role
of the FSA should be to protect and inform the public, not to
"reassure" it. As a safeguard it must insist on labelling,
traceability, monitoring and post-market surveillance of all GM
foodstuffs including derived products. The Lords rejected the
idea of an outright moratorium on commercial releases [2
paragraph 98], on the grounds it would allow our competitors to
get ahead, and that only large scale trials give information as
to how transgenic crops interact with the environment. A moratorium
would enable us to discover some of the problems from the releases
already occurring on a continental scale. In US with only 10 per
cent of its land in agriculture the impact of GMOs on ecosystems
is less damaging than on the patchwork agrisystems of Europe.
A moratorium would give us time to pause and think: should we
go down that road?
Nuclear energy was once considered safe and
cheap. We now know the costs of decommissioning and of nuclear
accidents make it neither safe nor cheap and could burden future
generations with pollution. GMO releases are similarly irreversible.
A safe and adequate food supply can be ensured for all if research
funds were diverted into ecologically sound agricultural technologies;
if land and income were sufficient for the poorest to grow or
buy their food; and if food sovereignty were guaranteed by international
law against the take-over of our food supplies by global corporations
and their legal arm the World Trade Organisation (WTO).
Our advisory bodies do not have the remit to
ask the questions: are the risks of GMOs necessary? are the benefits
long-term? are there alternatives? Everyone of us and every MP
should ask them. Our health and the future of our beautiful country
may depend on how we answer.
1 House of Lords Select Committee
on the European Communities. EC Regulation of Genetic Modification
in Agriculture. Session 1998-1999. 2nd Report. Evidence. HMSO
2 Ibid Report.
3 Jung C et al Engineering
nematode resistance in crop species. Trends in Plant Science 1998;
4 Gledhill M and McGrath P Call for
a spin doctor. New Scientist. 1 November 1997 p. 4.
5 Pusztai A SOAEFD Flexible Fund
Project RO 818. Report of Project Co-ordinator on data produced
at the Rowett Research Institute. October 1998.
6 Interim SCRI Report FF 818 April
7 Siva P K et al. Genome intruder
scanning and modulation systems and transgenic silencing. Trends
in Plant Science 1998; 3:97-105.
8 Kappeli O and Auberson L. How safe
is safe enough in plant genetic engineering? Trends in Plant Science
9 Ho W M Genetic EngineeringDream
or Nightmare? chapter 8 pp. 102-123. Bath; Gateway Books 1998.
10 Inose T and Murata K Enhanced
accumulation of toxic compound in yeast cells. Int J Food Science
and Technology 1995; 30:141.
11 Mayeno A N and Gleich G I Eosinophilia
myalgia syndrome and tryptophan production: a cautionary tale.
Trends in Biotechnology 1994; 12:346-352.
12 Bergelson J et al. Promiscuity
in transgenic plants. Nature 1998; 395:25
13 Jonathan Beard reporting in New
Scientist 8 March 1997 p. 5.
14 Hillbeck A et al. Effects
of transgenic Bacillus thuringiensis corn-fed prey on mortality
and development time of immature. Chrysoperla carnea. Environmental
entomology April 1998 p. 480.
15 Charlene Crabb reporting in New
Scientist 16 August 1997 p. 12.
16 Gordon A W et al. The potential
consequences of pollinator declines on the conservation of biodiversity
and stability of food crop yields. Conservation Biology 1998;