The Institute of Health and Environmental Research Inc.
PO
Box 155, Kensington Park SA, 5068.
of InVigor®
canola (DIR 021/2002)
The
Institute of Health and Environmental Research Inc (IHER) is making this
application to the Office of Gene Technology Regulator (OGTR) in relation to
the OGTR’s Risk Assessment and Risk Management Plan (RARMP), Consultation
Version, April 2003, DIR 021/2002. This
application covers an application for licence for dealings involving an
intentional commercial release into the environment of seven similar lines of
genetically modified (GM) canola covered by the registered trade name InVigor®,
by Bayer CropSciences Pty Ltd. These
lines are T45, Topas19/2, MS1, RF1, RF2, RF3 and MS8, and hybrids derived from
MSxRF crosses. They all contain
resistance to the herbicide glufosinate ammonium, four contain the
barnase/barstar fertility control system (MS1 and MS8 contain barnase, RF1, RF2
and RF3 contain barstar), and four contain DNA that codes for resistance to the
similar antibiotics kanamycin and neomycin (Topas 19/2, MS1, RF1 and RF2). The
lines that are proposed to be immediately commercialised in Australia are the
MS8 and RF3 lines.
The
Institute of Health and Environmental Research Inc. (IHER) is a newly
established research institute with an interest in GM organisms, particularly
those destined for food. Its directors
hold the following degrees: ordinary degrees in Medicine, Science and
Agriculture, Honours Degrees in Agricultural Science and Chemistry, a Master of
Public Health, and PhDs in Plant Genetics and Medicine. The Directors have
training and expertise in plant science, agriculture, medicine, chemistry,
biochemistry, nutrition, infectious disease, epidemiology and biostatistics.
The
OGTR’s definition of the environment is extremely narrow. To the OGTR, “the environment” seems to be
just natural, undisturbed ecosystems, of which there is very little remaining
in Australia. The rest of Australia,
including agricultural lands, disturbed lands or roadside verges do not seem to
be included in the definition, despite being parts of the Australian
environment.
As canola
seed is tiny, light, hard and electrostatically charged, it can easily be
carried by wind, water, animal fur (including sheep) and the faeces of animals
(including grazing animals) and birds. It can easily be disseminated from
vehicles used for harvesting and transportation to roadside verges and other
farmer’s lands. Because it is
electrostatically charged, it can even travel up the side of tarpaulins on
transport vehicles to be blown off the back of the vehicle. This results in contamination of roadside
verges. In many agricultural areas,
roadside verges contain most or all of the last remnants of rare and endangered
Australian native plants, simply because these areas are the only habitat
remaining to the plants in agricultural areas.
However, pollen is the
primary vector through which engineered genes can be transferred to
non-transgenic crops. Insect pollinated crops, such as canola have even greater
opportunities for cross-pollination between GM and non-GM crops than
wind-pollinated species. It is well known that bees can carry pollen over
distances in the order of 5 kilometres so that any non-GM crops within a 5 km
radius of a GM insect pollinated crop such as canola risk being pollinated by
GM pollen.
There is evidence that GM
crops have pollinated and contaminated non-GM crops. In North America, where
large areas of GM canola are grown, there have been several cases in which GM
pollen has cross fertilised non-GM crops resulting in GM seeds being harvested
from a supposedly non-GM crop (Hall et al, 2000). In Australia,
herbicide-tolerant canola has been detected 5 km from the source field (Rieger
et al, 2001). This provides evidence
that just a single commercial-like planting of GM canola under Australian
conditions can result in a spread of the GM canola for 5 km. It would be expected that each subsequent
generation would spread the GM canola the same type of distance again. Note
that a canola plant is capable of producing 7,000 seeds, of which approximately
10-20% fall onto the ground during harvest, to germinate some time over the
next approx. 10 years. Each seed can
then produce another 7,000 seeds, and so on, over an infinite number of
generations. This permits profound
exponential growth in the number of GM canola plants in the environment. Yet
the OGTR appears to be relying on a 5m buffer zone to prevent pollen flow
between GM and non-GM neighbours.
Furthermore, there is only a recommendation, not a requirement for GM
growers to tell their non-GM neighbours that they are growing GM canola. Many farmers may therefore grow a non-GM
crop (including canola) and be completely unaware of the potential for GM pollution
in their crop. However, once told,
non-GM growers are then required to go undertake the time-consuming and costly
procedures of maintaining 5m buffer zones, including harvesting and keeping
separate the canola in that zone. Such
as system is not designed to prevent the spread of GM canola in the Australian
environment.
In North America, the spread
of GM canola has created enormous legal problems for a number of North American
farmers who were found to have GM canola growing on their properties without
the required licensing agreements. There is anecdotal
evidence that 1,800 Canadian farmers are currently under investigation by one
of the proponents of GM crops for infringes of patent, and perhaps
40,000-50,000 have been investigated. In many cases, the GM canola most likely
contaminated the farmers’ paddocks through windborne seed or pollen. However
the courts have determined that it did not matter how the GM plants came to be
there, the fact that they were growing without a licence agreement was enough
to breach the genetic engineer’s property rights. These cases have been very
costly to the farmers concerned. In addition, the level of
contamination is such that farmers now essentially cannot get non-contaminated
seed, even when bought as certified seed.
Because
it is now almost impossible to grow non-GM canola in Canada without significant
contamination with GM canola, a group of organic farmers in Canada have lodged
a class action against Monsanto over the loss of their canola market. In fact,
any commercial release in Australia may result in a worse situation than
this. This is because, unlike Canada,
Australia does not have heavy frosts and snow to kill canola volunteers that
germinate in the autumn and does graze stock on crop stubble, a situation that
would significantly worsen the spread of GM seed.
The OGTR has acknowledged that this GM canola will spread beyond the
planted site. However, it has not
acknowledged that the widely-spread patented gene will likely cause similar
legal problems in Australia.
In
its RARMP, the OGTR acknowledges that there is evidence that volunteer GM
canola is difficult to control. That
is, Bayer CropSciences Pty Ltd was required to return to its trial sites to
remove volunteer GM canola after it had completed its trials. In fact in 2 sites, Bayer had to destroy the
subsequent non-canola crop in order to be able to destroy the GM canola
volunteers in the crop. Under a
commercial release, the removal of volunteers will not be required and the GM
canola will be permitted to grow on the same site in subsequent years and
through seed and pollen, to spread widely to public and private lands,
including national parks and roadside verges without any requirement for a
clean-up in those places. The OGTR has
tried to reassure us that canola cannot grow in national parks. However, it is clear from the OGTR document
that there are no scientific studies upon which to base this reassurance. The only study cited was an unpublished
study by a Monsanto employee, were the author asked National Park weeds
personnel if they had seen much canola.
This is hardly an independent, properly-conducted scientific survey of
canola plants. In addition, as part of
its reassurance that GM canola cannot be a weed the OGTR states that “canola having been bred as a cultivated
crop can only germinate and establish under optimal growing conditions within a
well managed agronomic system”. The
OGTR then contradicts itself by saying “canola occurs in disturbed habitats
along roadsides, railway lines, field margins and waste lands in all countries
where it is grown”. These places are
hardly optimal growing conditions within a well-managed agronomic system.
The OGTR acknowledges that
GM canola will cross-pollinate with non-GM canola and that the GM DNA in
InVigor® canola will move into the non-GM canola population. It also admits that “gene stacking” will
occur and that “multiple herbicide resistant canola volunteers will be
inevitable”. In Canada, gene stacking
has resulted in canola plants with resistance to three herbicides spreading through
the environment. Furthermore, there are
reports that at one trial site, a canola was generated that was resistant to
five herbicides through cross-pollination.
In Canada, 2,4-D and paraquat are being
recommended to control such volunteer multi-herbicide-resistant weeds. The OGTR
recommends similar control measures in Australia. The OGTR also states that “in
Canada where canola is grown no more than once in four years, surveys have
shown that the numbers surviving from the previous crop are less than one half
of one plant per square metre”. This
equates to one plant per 2 square metres, or 1 plant for every
dining-table-sized piece of land. This
is an enormous amount of volunteer GM canola and a correspondingly enormous
amount of 2,4-D will be needed to keep it under control. Hence, the OGTR is knowingly sentencing
Australia to repeat Canada’s awful experience.
Moreover,
even if no further commercial releases are granted, non-GM triazine and
imidazolinone-tolerant canola are currently widely grown, comprising
approximately 60% of the canola market.
There is therefore an opportunity for canola to be generated that is
resistant to 3 different herbicides without any further commercial releases of
GM canola. Further GM releases of
canola will only worsen the multiple herbicide resistant problem, creating
super weeds that cannot be killed by a wide range of herbicides. The IHER is
concerned that the OGTR is ignoring how bad the problem could get in Australia.
Of
particular concern, the OGTR describes multiple-herbicide resistant canola as a
“manageable risk”. It also suggests
that this “manageable risk” can be achieved using methods that are regarded as
impracticable on farms. For example, it
suggests thorough cleaning of equipment.
However, each thorough clean of harvesting equipment takes about a week,
something that is not practicable for contract harvesters between paddocks
during harvest. Even Bayer “recommends that farmers should anticipate multiple
herbicide resistance”. It then
recommends similar impracticable methods to minimise the potential. Inexplicably, The OGTR has also put Bayer in
charge of auditing it own stewardship strategy and has not required any
independent auditing.
The
OGTR then argues that the combination of widespread commercial growth and this
subsequent movement of seed and pollen via humans, animals, insects, wind and
water will NOT provide any adverse risk to the environment on the basis that
there will “not be any selective advantage over non-GM canola in the absence of
the herbicide”. This argument is flawed.
The OGTR document shows that this herbicide is already used to a
significant extent. For example it is
used in horticulture (particularly on grapevines, fruit trees and vegetables),
commercial and industrial areas, rights-of-way and other non-agricultural
areas. Widespread commercial growth of
InVigor® canola will naturally require the use of much larger amounts of this
herbicide. Like all sprayed herbicides,
it will be prone to spray drift of up to several kilometres. There will
therefore be strong selective pressure for this gene (and therefore this
canola) for several kilometres from every site in which it is commercially
grown, from spray drift alone. Note
that the distances for spray drift approximately match the distances of the
expected spread of canola from the planted site due to wind, water, pollen,
etc, allowing for selection of this GM canola in places where it is likely to
spread.
The
OGTR also relies on a flawed assumption that Bayer CropSciences will at no
time, now or in the future, apply to the Australian Pesticides and Veterinary
Medicines Authority (APVMA) for permission to use this herbicide more widely
than with its InVigor® canola. Once the
gene is released into the environment, it will remain there, possibly for
thousands of years, and any substantial use of this herbicide at any time in
the future could provide for selective pressure for that canola.
The
OGTR also relies on the flawed assumption that once farmers have legitimately
obtained glufosinate ammonium, they will not use it anywhere else on their
property or establish a black market in it.
Farmers may be very keen to use it more widely on their properties as
their weeds may not have had much exposure to this herbicide as yet, resulting
in good control of still-susceptible weeds.
In
conclusion, the OGTR has stated in its RARMP that “the risk of the GM canola
spreading as a weed in Australia is low”.
It is clear that this statement is wrong and that the opposite is in
fact true. The OGTR has also ignored
the consequences of this canola becoming a weed on Australian farms where the
farmer does not want to grow GM canola.
These farmers can be sued for growing a patented gene without a legal
agreement with Bayer. As a result of this
gene pollution, farmers may be forced to grow GM canola, and pay the licensing
fee, whether they want to or not, particularly once they are unable to source
non-contaminated seed.
In evolutionary terms, most
crop species evolved recently. They developed larger and more palatable seeds
and fruits than their wild relatives 5,000 to 10,000 years ago with the
development of agriculture and the repetitive selection of the largest and
tastiest crops by the first farmers. Because crop species have only recently
evolved, cross pollination is possible between many crops and their wild
relatives. Although the evolutionary
distance between them often means that inter-specific cross pollination is less
successful than cross pollination within the crop, the growth of millions of GM
canola plants greatly increases the probability that some GM DNA will be
transferred to similar species that are grown nearby.
Experiments have shown that
engineered genes from canola are easily transferred to other canolas (Brassica rapa), including rape and the
weedy relative Brassica campestris (Mikkelsen
et al, 1996). Canola is also capable of
cross pollinating with several other weed species including wild raddish (Raphanus raphanistrum), buchan weed (Hirschfeldia incana) and Sinapsis arvensis and can pollinate
related crop species including broccoli, cauliflower, cabbage (Brassica oleracea), mustard (Brassica juncea), swedes, rutabaga,
Brussel sprouts, kohlrabi and Siberian kale, amongst others (Salisbury, 2002;
OGTR, 2003).
The
OGTR determined that if such gene transfer did occur, there would not be any
increased risk to weediness because glufosinate ammonium is not used to control
these plants. This ignores the fact
that these weed species tend to grow in the same locations as canola. Spray drift and the possible use of
glufosinate ammonium by farmers on sites other than the GM canola field would
provide selective pressure for GM weeds over non-GM weeds. The subsequent introduction of other
herbicide-resistant canolas (whether GM or not), would confer resistance to
even more herbicides in these weeds.
The
OGTR also ignores that fact that if GM DNA transferred to food crops such as
broccoli and cauliflower, a situation that would be expected over the next few
years, these new GM foods would be entering the human food supply without any
approval or safety assessment. The
OGTR argues that this would be rare based on the fact that farmers growing these
crops harvest their crops before they seed.
However, this ignores the fact that many farmers allow part of their
crop to progress to seed in order to produce seed for following years. The GM canola crop just needs to be within
bee-flight distance (approximately 5 km) of any GM canola including roadside
volunteers. In addition, the overseas
legal finding is that wherever the patented gene lands, it belongs to the
company that owns the gene. This may
cause crops such as broccoli and cauliflower that contain the GM DNA to be
owned by the patent-holder.
The OGTR in
its RARMP, estimates that gene transfer from the GM canola to closely-related
species to be “very low”. It is clear that the OGTR has ignored clear evidence
that this statement is wrong and that the opposite is in fact true.
The
movement of genes between species outside of the normal reproductive process is
referred to as “horizontal gene transfer”. One examples of horizontal gene
transfer in nature is the transfer of DNA from the HIV retrovirus into human
DNA to cause disease. Another example is crown gall disease of stone fruits
where the bacterium Agrobacterium
tumefaciens transfers some of its DNA into the plant’s DNA causing disease.
Genetic engineering is an artificial form of horizontal gene transfer, where
genes may be transferred between species.
There
also exists potential for transgenes to be transferred across wider species
boundaries. The likelihood of these events may be quite low but the potential
nevertheless exists and should be examined thoroughly. It should also be
remembered that even unlikely events increase in probability with multiple
replications. Consequently, as the
number of different types of transgenic organisms released increases,
and the number within each type increases (eg the amount of InVigor® canola
planted increases), so too will the probability of unlikely genetic
recombination events.
Genes
are not as static as once thought. It has long been known that genes are
transferred with relative ease between different species of bacteria. Gene
transfer from viruses to host species of plants, animals, bacteria and fungi
has also been frequently observed. In Contrast to the
OGTR stance, there
is now very good evidence that functional genes may also be transferred from
plant tissue to fungi in soil, between bacteria and plants and between bacteria
and fungi. For example, there have been
several examples of the transfer of genes from plants to fungi or bacteria. There are concerns that transgenic DNA could be involved in this process
more readily than normal DNA, due to the nature of the gene sequences, in
particular the gene switches which are designed to allow integration of foreign
genes into a host. Already, engineered genes introduced
into Datura, Brassica, and Vicia
species have been shown to be transferred to the fungus Aspergillus niger (Hoffmann et al, 1994).
In contrast to the OGTR position, there is also good
evidence of transfer of GM DNA from plants to animals. Some have pointed-out
that transgenic DNA is specifically designed to cross species barriers and to
jump into other genomes (Ho, 2002). In fact, in vitro human simulations
indicate that transgenes in GM food may survive in the human stomach and small
bowel for up to four hours (Martin-Orue et al, 2002). Furthermore, an oral
bacterium was found to take-up and express free exogenous DNA within only a
minute (Flint and Scott, 2002). In addition, foreign DNA ingested by mice can
reach peripheral leukocytes (a type of white blood cell), spleen and liver via
the intestinal wall mucosa and can be found in B and T cells of the immune
system and covalently linked to mouse DNA (Schubbert et al, 1997). Other work
has indicated that short DNA fragments from plant chloroplasts can be found in
the lymphocytes of cows, and possibly in their milk, while muscle, liver,
spleen, and kidney tissues from chickens were found not only to contain, but to
amplify, certain gene fragments (Einspanier et al, 2001).
In addition, in the only GM food study that could be
found on humans, seven people, who had previously had their lower intestine
removed and consequently used colostomy bags, were fed a single meal of a
burger and milkshake both containing GM soy. It was found that ‘a relatively
large proportion of genetically modified DNA survived the passage through the
small bowel’ (Netherwood et al, no date given on the UK Food Standards Agency
website). There was also evidence of genes being transferred from the GM soy to
intestinal microbes (Netherwood et al, no date given on the UK Food Standards
Agency website). It is also known that
several bacteria can invade intestinal cells and transfer genes into mammalian
cells (Food Standards Agency, no date). Furthermore, GM DNA has been found in
rat faeces for up to 79 hours after feeding the rats naked GM DNA (Flint et al,
2001).
So,
once a novel DNA is introduced into a crop there is potential for it to escape
not only to related weed species but to completely different types of
organisms, including animals and for those animals to shed the GM DNA in their
faeces. The evaluation of such an
transfer into a single species on the environment is very difficult to
evaluate. The evaluation becomes
exponentially more difficult if the gene is also readily on-transferred to other
species. This is a particular concern in the soil ecosystem where there are
abundant and diverse micro-organisms in close proximity with the potential for
gene exchange and where scientists are only beginning to come to terms with the
extraordinary complexity of the soil ecosystem.
In conclusion,
the OGTR’s view that gene transfer from the GM canola to widely divergent
species in the environment is “very low” is wrong and that the OGTR has ignored
evidence on this matter. Horizontal
gene transfer does occur and would be expected to occur over time with this
canola. The possible effects of this
have not been determined.
The
introduction of a gene into a plant cell using genetic engineering is a very
hit-and-miss affair with many target cells not expressing the gene at all and
some cells expressing multiple copies at various levels of expression depending
on where the new gene or genes are incorporated into the host chromosomes. As
the inserts are placed indiscriminately, some may be placed where they affect
the expression of the plant’s genes. This may turn genes off, or on, affect the
function of other genes, produce new toxins or allergens, or produce a ‘wild
characteristic’ such as higher levels of toxins found in a wild ancestor.
Unfortunately,
this may have occurred with these canolas.
They provide evidence that line RF3 has one full copy and a partial copy
of the genetic insert, while Topas 19/2 has one copy and an inverted copy of
the inserted DNA. Because Bayer
CropScience provided Southern blot analyses but not Northern blot analyses, it
cannot be determined that the canola has not produced new substances as a
result of this insertion. Furthermore,
the OGTR believes that its document indicates that the genetic insert into RF3
has gone into a non-coding region of the canola DNA. However, as we do not know all of the genes in canola, this
cannot be demonstrated to be the case.
Even worse, the flanking regions of MS1, RF1 and RF2 clearly indicate
that the genetic insert has gone into a coding region of the canola. But because the function of that region is
not as yet known, the OGTR has assumed that the insert will not change the
genetic expression of the canola and that no new substances will be
produced. This is very dangerous
ground, indeed.
Of
additional concern, the OGTR relies on Bayer’s results from ELISA tests that
various proteins that were genetically engineered to appear were not detected
in various plant products. For example
Bayer could not find PAT protein in canola oil nor NPTII protein in seed. However, the OGTR document (OGTR, 2003) then
stated that the Canadian Food Inspection Agency had found the NPTII protein in
seed and that Bayer had stated that the values found by the Agency were below
the limit of detection of Bayer’s tests.
This suggests that Bayer’s tests were insufficiently sensitive and that
these proteins may be found with more sensitive tests. Yet the OGTR did not require the more
sensitive tests to be undertaken in order to aid its decision.
Because
the site of incorporation cannot be determined in advance and because viral
gene promoter sequences (eg from cauliflower mosaic virus) are frequently used,
there is a small but real possibility that latent viral or transposable element
sequences residing the plant genome could recombine with the introduced genes
to produce new transcripts which could produce new viruses. In addition, there is a risk that viruses
which attack GM plants may combine their genes with the engineered gene to
create viruses with new characteristics such as increased virulence on the host
or the ability to infect different species (Schoelz et al, 1993; Rubio et al,
1999). There are also studies which suggest that expressed transgenic viral
coat proteins can encapsidate DNA or RNA from other infecting viruses.
The
Cauliflower Mosaic Virus (CaMV) is a specific cause for concern. The OGTR has
tried to discount concerns about this and other “eukaryotic regulatory
sequences” by stating that “even if any of these transgenes were transferred to
bacteria, it is highly unlikely that they would be expressed”. However, there is evidence that at least
CaMV is able to function in algae, plants, animals and mammals including
humans. It
is also able to recombine with a wide range of hosts, including
micro-organisms, plants, and animals. It has also recently been demonstrated that it contains
a recombination “hot-spot” where recombination with non-homologous or genetically
different DNA sequences occur more frequently. This increases the likelihood of
recombination with invading viral DNA. It may also lead to unpredictable gene expression, and hence wide
disruption to eco-systems. Early evidence from Mexico (where GM corn has been
banned to conserve its ancient strains of maize) shows that landrace corn has
been contaminated with CaMV.
Furthermore, there is evidence that the contamination was in the form of
a scrambled gene sequences present, which is consistent with having been
acquired by horizontal gene transfer. If this is true, strains of InVigor®
canola may irreversibly damage biodiversity and make it almost impossible to
conserve all other crop strains.
The
OGTR reports that these were “no adverse effects” reported, but it appears that
this conclusion was reached without any scientific studies into the animal
populations and no surveillance of them.
This is therefore a highly suspect conclusion.
Effect of this GM canola on
insect populations
The
only quoted studies on insects were done overseas. None appear to have been done in Australia with Australian
insects under Australian climatic conditions.
The OGTR just states that Bayer has stated that there have been “no
effects on native species present near trial sites or abundance of prey or
parasites at any of the trial sites conducted to date in Australia”. However this seems to be an unscientific
observation. There is no reference to
any scientific study to back-up these claims.
Canola
is pollinated by bees and other pollinating insects. The OGTR states that “no
differences [were observed] between the behaviour and health of bees foraging
on the GM canola lines or non-GM canola”.
However, much of this is based on statements from agencies that did not
do their own studies. In fact, it
appears that only a tiny number of studies were done on the effects of GM
canola on bees and only one of these was published in the peer-reviewed
literature. It is not clear whether
this was done on small trial sites, where bees can easily choose other pollen
sources or on commercial release sites, where the bees have little choice but
to feed on canola. There appear to be no studies done in Australia using
Australian bees under Australian climatic and foraging conditions.
However,
in spite of this profound lack of information, the OGTR has decided that there
will be no risk to Australian insects including bees or their hives.
Soil health is
critically dependent on soil micro-organisms.
However, we know very little about these organisms, so little in fact
that many have not yet even
been allocated scientific names.
Because of our profound lack of knowledge of these organisms, the use of
GM plants could have unforseen effects on them. In particular, the short and
long term impacts of this particular GM plant on soil organisms have not been
determined and are therefore unknown. Recent evidence is that GM sugarbeet
DNA coding for antibiotic resistance persists in soil for at least two years,
and it is transferred into soil micro-organisms. Another concern is the impact of chemicals applied to crops
engineered to be resistant to various herbicides. GM herbicide resistant
varieties sold as a package with proprietary herbicides encourage increased use
of specific herbicides, whose impact on Australian soil flora and fauna is
unknown.
It is therefore of concern that the OGTR bases it assessment that there
would be little adverse effect on soil organisms on the basis of a tiny number
of studies, none of which were done in Australia using Australian soil
organisms under Australian climatic conditions. Of additional concern is that that results from overseas that
this GM crop may have adverse effects on soil organisms that appear not to have
been further investigated.
Environmental monitoring and
surveillance
One
of the reasons the OGTR gives for permitting a commercial release of this
canola is that no adverse effects on the environment were reported during the
trial releases. But these statements
appear not to be based on proper studies or surveillance. Furthermore, the OGTR is proposing minimal
oversight conditions on any commercial release which do not include any
conditions or provisions for monitoring, surveillance or scientific studies of
the introduced gene in the environment (including gene transfer to other plants
and to microbes in the soil), animals (including farm animals) or humans. The
OGTR states that it will review the commercial release if there is evidence of
harm to the environment or human health.
However, it then chose a system of regulation of this canola that
excluded conditions or provisions that would determine if this harm was
occurring. The IHER regards this as negligent.
The OGTR relies considerably on the fact that some other countries have
approved the oils from these canolas for human consumption. It is important that the OGTR recognise that
these approvals are up to 8 years ago, when far less was known about genetic
engineering than today. It is also
important to note that many of these approvals were granted on the basis that
the USA’s FDA gave the original approval, and that it approved the consumption
of GM foods on the basis of a political directive rather than a proper safety
assessment. At the time, it seems that
there was not even any requirement for the applicant company to lodge its
safety data with the FDA. The approval overrode the warnings of the FDA’s own
experts that further testing was needed.
The relevant FDA documents can
be seen on www.biointegrity.org.
It is also important that the OGTR recognises that other countries have
not approved these canolas for use.
Included is China, a major importer of Australian canola.
The OGTR relies considerably on the fact that ANZFA/FSANZ has approved
the oil from these canolas as safe for human consumption. It is important for the OGTR to recognise
that FSANZ has done none of its own safety testing, instead relying on the company data.
It has however produced a document describing its guidelines for assessing
safety of GM foods (ANZFA, 2000), which are best described as safe until proven
harmful, the opposite of a precautionary approach. Perhaps the agency is
constricted by its mandate, which is to both protect public health and safety
and to promote fair trade, trade and commerce, and consistency between domestic
and international regulations. It is
also important to recognise that the peak public health body
in Australia, the Public Health Association of Australia (PHAA), has for years
strongly criticised the quality of these safety assessments and has advocated
for far more comprehensive assessments, including writing to all the health
ministers in Australia requesting this.
The OGTR has stated that the metabolites of glufosinate ammonium are not
toxic. However, glufosinate ammonium
inhibits glutamine synthetase, which catalyses the following reaction:
L-glutamate + ATP + NH3 → L-glutamine + ADP + Pi. In plants, inhibiting glutamine synthetase
causes accumulation of ammonia and hence causes severe damage to plant tissues,
killing the plant (OGTR, 2003).
However, what the OGTR document does not say is that glutamine
synthetase is also an important means of removing ammonia in humans. Ammonia is toxic at very low levels in
humans (ie above 4x10-5 M in blood) (Brownie and Kernohan,
1999). The enzyme is also of central
importance in the net synthesis of the nitrogen-containing groups of
nitrogenous cell constituents such as amino acids, amides, carbamyl and guanido
compounds in humans. Glufosinate is a recognised neurotoxin and there are concerns that male agricultural workers
may have a higher rate of congenital malformation in their children as a
result. It is self-evident that permitting the commercial release of a canola
that is resistant to glufosinate will greatly increase the use of that
herbicide. In addition, the development of multiple herbicide-resistant weeds
will require the use of even more toxic herbicides to kill them, e.g. 2, 4-D
and paraquat.
The increased use of these herbicides on human health in Australia have
not been assessed. In particular,
InVigor® canola is designed so that glufosinate ammonium can be sprayed on the
canola plant after it has emerged and is growing. Therefore more of this herbicide (and its associated surfactant)
are likely to be present in the GM canola plant at harvest than in non-GM
canola. As herbicides and surfactants
are generally fat soluble, it is expected that any increased levels of these it
will enter the canola oil which people eat.
The risks to people from this greater exposure have not been
assessed. The ability of this herbicide
and its surfactant to move through Australian soil and water systems also do
not appear to have been assessed.
Furthermore, multi-herbicide resistant canolas will likely require the
application of several different herbicides to kill them. The environmental and health effects of this
have not been assessed. Finally, 2,4-D
contains traces of dioxin, and the extra exposure from this to the Australian
environment and population have also not been assessed.
GM sterile crops use barnase, an enzyme which destroys RNA. RNA is the essential link between DNA and its
functions in all living cells. Barnase is a non-specific poison, capable of
killing any cell exposed to it. Obviously, every cell in the plant will contain
the barnase gene, which will only be expressed in its reproductive organs. This
means there will be billions of copies of the gene for barnase in even a small
field of this canola. This new (plant) environment has provided the barnase
gene with new opportunities for gene transfer to organisms that may not
previously have occurred. The consequences of this could be absolutely awful.
Genes
coding for antibiotic resistance are used as selectable markers for transgenic
plant production. This provides
organisms, including humans to unnatural and unprecedented exposure to new
sources of antibiotic resistance genes.
These GM canola plants confer resistance to
aminoglycoside antibiotics such as antibiotics, kanamycin, gentamicin and
neomycin. The OGTR has sated that
neomycin and gentamicin are infrequently used. This is news indeed to several
clinicians and hospital scientists that specialise in the area that were
contacted by the IHER. Neomycin is used
occasionally as a topical antibiotic in medicine. Gentamicin is not used for trivial infections because it is
reserved for seriously ill hospitalised patients for serious conditions such as
complicated urinary tract infections, septicaemia, burns, infected wounds, bone
and soft tissue infections, including peritonitis. It is widely used in these
applications, particularly for people who are risk of death due to septicaemia.
Such is the concern about antibiotic resistance in the medical community, that
some gentamicin-like antibiotics are kept in reserve, not to be used until last
resort. Amikacin is one of these. The experts contacted were highly concerned
that widespread use of the NPTII enzyme may place the use of these highly
reserved antibiotics at risk as well.
It should be remembered that the InVigor® canola meal will be fed to
animals in intensive husbandry. In these
conditions it is routine to constantly feed antibiotics to animals as both a
growth promoter and as a preventative prophylaxis. These conditions have the highest potential to spread antibiotic
genes to bacteria. From there is only a
matter of time until antibiotic resistance is found in bacteria in people. The
OGTR also stated that the NPTII enzyme is so non-specific that it can
inactivate aminoglycoside and butirosin antibiotics but is somehow so specific
that it can discern between different sub-types of one of these antibiotics,
gentamicin. The OGTR provides no reference for such an interesting statement.
The antibiotic resistance was put in the plant in order to be able to grow it
in the presence of gentamicin as a selective marker. Unless Bayer has access to special, pure subtypes of gentamicin
that specialist clinicians and hospital scientists have not heard of, it would
have used “normal” gentamicin, which indicates that the NPTII enzyme can indeed
inactivate clinically-used gentamicin.
Moreover, cross-resistance has been demonstrated between different
aminoglycoside antibiotics and even between different classes of antibiotics.
There is a considerable lack of understanding about
antibiotic resistance, how it develops and how it is transferred between
organisms. However, there is some
evidence that once a bacterium has acquired one gene for antibiotic resistance
it is more likely to be able to acquire others. The significance of this is that even using a gene for resistance
to an obscure antibiotic may ultimately increase resistance to clinically
significant antibiotics. For these
reasons, the OGTR should take great care about allowing genes that confer
resistance to antibiotics to be widely grown in a commercial release of GM
plants.
The OGTR quotes widely from papers and documents written by Bayer and Monsanto-paid scientists. Many have not even been published. If the OGTR had done a proper literature search and consulted a FAO document, they may have been better informed.
The sequence homology approach accepted by the OGTR to determine whether the GM food is allergenic is regarded by the FAO as only the first of several steps to indicate whether the GM food is allergenic (FAO, 2001). The other steps have not been undertaken for InVigor® canola. Moreover, the FAO points-out that the protein and gene databases used for homology testing are often not up to date and hence cannot be relied-upon. Furthermore, little is known about the actual proteins that cause allergy, even for peanut allergy, one of the most serious and well-documented food allergies. For example, there appear to be “less than ten” protein fractions that cause peanut allergy (Sampson et al 1998). Given this lack of understanding, it is inadequate to consider that a comparison of the sequence homology of new proteins in GM plants to sequences of known allergens will be sufficient to determine whether a new protein is allergenic.
Furthermore, one of the key reasons why the OGTR found that oils from InVigor® canola was safe for humans was that canola oil does not contain protein. This is completely untrue. It has long been recognised that oils contain proteins (McCance and Widdowson, various editions). In fact, different brands of oil in the USA contain between 2 and 62 μg/ml protein (Moneret-Vautrin et al, 1998), which is sufficient to cause an allergic reaction in sensitive people. In fact, in an oral provocation test, 22% of patients allergic to peanuts reacted to peanut oil (Moneret-Vautrin et al, 1998). Moreover, there is evidence that allergy to peanut oil may be the main cause of anaphylactic reactions in England.
It is also important to consider that if oils contain
protein, they are also likely to contain small sections of DNA. Under these circumstances, horizontal gene
transfer between InVigor® canola and humans needs to be considered. In the light of the evidence above that this
event occurs with GM soy after only a single meal, the awful potential of a bacterium
in the gut taking up the gene for barnase needs to be considered.
Pollen is known to cause hay fever, asthma and allergies due to specific proteins expressed in the pollen. When new proteins are introduced into plants through genetic engineering, it is essential to test whether these proteins occur in pollen and to assess their allergenicity when inhaled as pollen. For example, a protein which is found in soil bacteria may not cause an allergic response on hands but may cause an allergic response when inhaled. In addition, honey will become contaminated with GM pollen and the allergenicity of oral GM pollen should also have been assessed. Based on the tiny amount of protein required to elicit an allergic response from oil, the amount of GM proteins in pollen in honey may also cause an allergic reaction.
In addition, the OGTR states that that allergenicity is unlikely to GM plants because humans are frequently exposed to these novel proteins, because the proteins are derived from common bacteria in the environment. Unfortunately, the opposite is true. People develop allergies to certain proteins because they get exposed to those proteins. Moreover, the allergic reaction tends to get worse with continued exposure.
As the OGTR document states, ‘compositional analyses
can provide evidence of whether any unintended effects have been introduced
into the GM canola lines as a result of the genetic modifications”. It is therefore of concern that the
compositional analyses as reported in the OGTR document, were so poor. They
appear to be even worse than ANZFA/FSANZ safely assessment documents, which the
PHAA has previously strongly criticised.
For example, the OGTR only presented data for fatty acid compositions.
There have been concerns expressed about possible novel proteins in GM plants,
and the IHER feels that an amino acid analysis should have been undertaken and
presented to review. As stated above,
oils contain proteins and therefore, these oils may contain novel proteins.
In addition, of the 7 canolas and the many potential
hybrids that are being assessed, the OGTR has given an analysis of only 2
canolas (MS8 and RF3) and 1 hybrid (MS8xRF3).
Two of the tables do not mention whether the canola was sprayed with
glufosinate ammonium or not. In two
tables, the data are given as a single number, with no indication as to whether
this is a mean or a median. No
indication is given as to the number of samples used to obtain these, standard
deviations or a 95% confidence intervals of the mean. In the other table, a range is given and the following are not
given: means, standard deviations, sample sizes and 95% confidence intervals of
the mean. When statistical tests are
mentioned, the following are not given: the sample sizes for each sample,
p-values and the nature of the statistical tests used. Peer-reviewed scientific
journals would require most or all of these or the paper would be rejected for
publication. Similar non-parametric
statistics would be required if the data are not normally distributed. Why have these not been given? Their omission prevents a full assessment of
the data by others. For example, when
no means and standard deviations are given, sample size calculations cannot be
done by others to determine at which sample size the comparison would have
become significant.
The FSANZ document on these canolas (ANZFA, 2001) also
uses information provided to it by Bayer CropScience. The document mentions only one sample size in one table; a sample
size of 6. With such low numbers it is
almost a foregone conclusion that a statistically significant difference will
NOT be found between the GM food and the non-GM food for most analyses, even if
one exists in nature. A much more suitable sample size would have been at least
n=50 to obtain an accurate picture of the compositional analysis of these
foods, and that on the basis of these results, sample size calculations should
have been performed to determine the number of plants that would be required to
find statistical significance at an alpha of 0.05 and a power of 80% and
90%. However, it appears that this was
never done. Bayer CropScience should
then have undertaken these analyses at the indicated sample sizes, and all of
the results should have been published in peer-reviewed journals for scientific
discussion before submission to the OGTR.
The IHER is concerned as to why such small numbers of
samples were taken, given that at the time, Bayer had field trials in operation
that must have totalled hundreds to thousands of plants. In addition, the
methodology of how plants were chosen should be provided, including whether
they were randomly sampled.
The OGTR document states that “although some
differences were observed [between the GM and the non-GM canolas], the
variation across environmental conditions was greater than any variation
between GM and non-GM canola plants”. Why weren’t the results analysed to
statistically control for the environmental conditions, so that the
compositions of the GM and non-GM canolas could be directly compared? Then the consequences
of the genetic engineering on the composition of the canola could be properly
determined. Instead, the results were
analysed in a way that allowed the variability of widely-differing site
conditions (eg soil, air temperature, rainfall, fertiliser) to enter the
analyses. This made any significant
difference between the GM and non-GM canolas almost impossible to find, even if
there was a real difference in nature.
This is exacerbated with small sample sizes.
In addition, when “some differences” were observed,
Bayer CropSciences did not follow-up these results with substantial further
experimentation to determine why these differences occurred. Instead, such differences in composition
tend to be dismissed as being within the natural variation of the plant.
The whole of the OGTR’s
document has an underlying hypothesis, that that the only new substances that
would be found in GM crops are the new substances that have been genetically
engineered to appear and that the plant will not produce anything else. This is an untested hypothesis for InVigor®
canola and all GM crops. It should be
noted that unexpected substances have previously been known to appear in GM
plants. For example, a tobacco plant,
genetically engineered to produce gamma linoleic acid also unexpectedly
produced a substance never before seen in tobacco plants: octodecatetraenoic
acid.
There are particular concerns about the production of any novel substances that are proteins. It is well known that proteins can cross the gut wall into bodily tissues to create toxicological and other health problems. Food allergies—for example, to peanuts—can kill susceptible people (Foucard and Malmheden Yman, 1999), and eating meat from cattle with bovine spongiform encephalopathy (BSE or mad cow disease) can kill people by causing variant Creutzfeldt-Jakob disease.
The OGTR also has a
stance that the DNA engineered into the plants, the organisms from which they
come and the substances that they produce are safe because they are already in
the environment. A similar argument
would be that Legionella, Salmonella, “golden staph”, cyanide,
ricin, botulinus toxin and prions are all safe because they are found naturally
in the environment.
As a result of these underlying, incorrect hypotheses,
the only toxicology studies undertaken were of the new proteins expected to be
found. The OGTR also believes that
because these proteins may have been in the human environment at some stage,
they are more likely to be safe for humans to be exposed-to. However, humans have not been exposed to
these proteins in such high concentrations in these types of exposure for this
long before. In addition, these studies were only
short-term toxicology studies. No
long-term toxicology studies were undertaken.
This is of concern as these proteins may be harmful to human health when
consumed in regular doses over a long period of time.
In addition, the type of testing undertaken assumes
that the GM plant-produced substance will act in the same manner as the tested
substance which is often obtained from another source, such as a bacterium
genetically engineered to produce it.
It needs to be noted that plants often add sugars and other substances
to their proteins so that they have a different composition to these proteins
obtained from bacteria. Consequently,
the proteins tested may in fact not have had the same chemical composition to
the substances produced in plants. The
tested substance also appears to be different to the PAT protein produced in
lines RF1, RF2, RF3, MS1 and MS8. It
was modified by Bayer to be different by 2 amino acids. In addition, for a 14-day toxicology study,
the PAT protein tested had a series of histidine residues attached to it
compared to “normal” PAT protein.
The final assumption is that the tested substance will have an effect on the test animal within a few days. Such an assumption is very dangerous. On the basis of these tests, tobacco, alcohol, asbestos, prions and thalidomide would all be regarded as safe.
The OGTR also relies on Bayer’s degradation experiments on expected novel proteins that are purported to show how quickly digested these proteins are. The OGTR is reminded how inaccurate these in vitro simulations are to in vivo reality. A useful example are the similarly-conducted in vitro experiments that concluded that GM DNA in GM soy would quickly degrade in the stomach. The results in humans however, were vastly different. Not only did “a relatively large proportion of genetically modified DNA” survive digestion in the stomach, but it also “survived the passage through the small bowel” (Netherwood, et al, no date given on the UK Food Standards Agency website).
It is therefore regrettable that largely on the basis
of these flawed tests, the OGTR has decided that there are no toxicology
concerns with InVigor® canola for soil microbes, insects (including bees),
animals (native, introduced or farmed) and humans.
Because these were so badly summarised in the OGTR document, the IHER had had to refer to the FSANZ document on these feeding studies to gain further information.
Of the 7 canolas and the many potential hybrids that
are being assessed, feeding studies are reported for only 1 canola (Topas 19/2
on chickens) and 2 hybrids (RF1xMS1 and RF3xMS8 on rabbits and canaries). In
addition, the fraction that is fed to humans, the canola oil, was not fed to
animals. Rather, canola seed was used,
which humans do not eat. FSANZ has
previously argued that studies feeding oils to animals may cause nutritional
and biochemical imbalances and hence are inappropriate. However, a review of the nutritional
literature shows that they are not only appropriate, but often conducted.
Furthermore, only one of these studies used
significant numbers of animals (280 commercial strain broiler chickens), but
these were only male chickens fed for 42 days and only body weight, feed
intake, mortality, chilled carcass weight and deboned breast meat yield were
measured. A study on rabbits (a low
number of 10 rabbits per diet) were only measured over 4 days and faecal
samples were taken and analysed to determine the digestibility of the seed and
“zootechnical performance” of the canola seeds. Note that this limited rabbit study is the only one conducted on
the hybrid expected to be grown immediately in Australia. Also note that there is a contradiction
between the OGTR and FSANZ documents.
The OGTR document mentions 2 feeding studies on rabbits, whereas the
FSANZ document mentions only one (it does not mention the hybrid selected for
widespread commercial production in Australia) and does not mention a feeding
study on canaries at all. The OGTR
document states that for the canary study, food consumption, behaviour or body
weight were measured. No mention was made
of the number of canaries per group or how long they were fed.
Chickens, rabbits and canaries are very unusual
animal models for human health. Some of the measurements taken from these
animals are also unusual measures of human health, such as chilled carcass
weight, deboned breast meat yield and faecal composition. It can only be concluded that these tests
have not been set-up to measure human health at all, but rather to reassure
primary producers that GM feed will permit farm animals to grow sufficiently to
get a reasonable price at market (rabbits are farmed overseas). However, in its
safety assessment, the OGTR remarkably uses these kinds of experiments as
evidence that these foods are safe for human consumption. What is even worse is
that the only results that could be translated to humans from these experiments
were death, food intake and body weight. These are profoundly crude measures of
human health. On the basis of these
kinds of tests, tobacco, alcohol, asbestos, thalidomide and chronic heavy metal
exposure would all be regarded as safe. Important tests such as biochemistry,
immunology, tissue pathology, and gut, liver and kidney function and microscopy
results were not given, and were therefore probably not done. In addition,
animals were not fed for long enough for cancer studies, or studies into the
effect of offspring, to be done. Consequently, those experiments could be
regarded as initial experiments in what should have been a long series,
starting with several thorough animal experiments and finishing with several
detailed human experiments, yet they remain the only ones done. On the basis of these tests, it is
recklessly negligent of the OGTR to regard oil from these canolas as safe for
human consumption.
It is
clear that InVigor® canolas have not passed human safety tests. In fact, they have never even been safety
tested on humans. In particular, these
canolas have not undergone the safety rigours of a clinical trial. Before a clinical trial is
even begun, thorough animal testing is undertaken to determine adverse and
therapeutic effects of the treatment in those animals. If the tests are passed,
the four phases of the clinical trial begin. Phase I tests for adverse effects
in a small number of healthy volunteers, Phase II tests for the therapeutic
effect in a small number of volunteers, and Phase III is the randomised
controlled trial (RCT). If the new treatment passes all these steps, it is then
monitored in the community (Phase IV).
As a result of the push towards ‘evidence-based medicine’ a further step
is often undertaken, the meta-analysis. This process statistically sums the
results of a number of randomised controlled trials to get a better
picture. It is clear that InVigor®
canolas have not even completed the pre-clinical trial animal testing stage of
this process. No reasons are given for this lack of safety testing. It is of
concern that in the face of this overwhelming lack of evidence of safety, the
OGTR unwisely still regards these canolas as safe for humans.
However,
even these studies cannot determine the long-term health effects of GM foods on
humans. To do this, long-term cohort studies are required, where people’s
current self-selected exposure to various GM foods are measured over future years
and any diseases noted as they arise. In addition, specific surveillance
systems would be required to pick-up any ill-health effects in the general
population.
Instead,
the OGTR relies on Bayer’s self-report that their employees did not show
“changed allergic reactions in annual medical examinations”. No information is given as to whether
baseline measurements were taken before employment, what measurements were
taken at the examinations (allergies are rarely measured at medical
examinations), if allergies were measured, how they were measured (specific
measurements on blood would need to be undertaken), whether those who left
before a yearly examination were chased-up for their reasons for leaving (were
there medical reasons?), etc. Little
mention is made of the fact that it is in the interests of employees to
demonstrate their good health to an employer in order to continue their
employment. In short, this is not a
properly-conducted study. There is too
much bias. Only a properly-conducted
epidemiological study on a large number of people can determine the
relationship between exposure to InVigor® canola and adverse health. This Bayer report is not it.
It is also clear that
these canolas have not been designed for any benefit to humans. Consequently it would only require a small
adverse effect on people for any harm to completely outweigh the (nil) benefit.
In the face of this
profound lack of information, the IHER believes it is recklessly negligent to
consider InVigor® sufficiently safe to permit 19 million Australians to be
exposed to it, either directly in fields, via pollen or in food.
One
of the reasons that OGTR gives for finding this canola safe for humans is that
there have been no reports of adverse effects on human health reported from
this canola. However it is clear from
the OGTR document that there may have been no system in place to report any
adverse events. That is, there has been no proper attempt at surveillance and
monitoring. It is also clear that there
have not been any epidemiological studies into the effects of InVigor® canola
on human health.
It is also of
concern that the OGTR appears to be using the same argument as proponents of GM
food and the FSANZ, that because no-one has found any documented cases of
people who have gotten ill from eating GM food, then GM food must be safe. This is completely unrealistic. Unfortunately, there may be many cases of
illness from exposure to GMOs that we are unaware of because we have inadequate
general surveillance systems, no-one is being paid to look at those
surveillance systems for cases and there is a complete lack of a specific
surveillance system for GMOs. Furthermore, if exposure to a GMO causes a novel
illness, then by definition, we do not have a surveillance system to pick it
up. In addition, because of the lack of
full animal testing, we don’t even know which diseases to look for in our
general surveillance systems, such as hospital separations databases. Consequently, we may be sitting on a big
problem that we are completely unaware-of.
This happened with HIV/AIDS for decades, and even today, we still don’t
know how many cases of this disease there are.
Finding cases
of illness is however only the first step. Then a team of epidemiologists would
need to prove that GM food was the cause by mounting an investigation, because
surveillance only indicates there is a disease. It does not inform us of the
cause. This would require an application for a considerable amount of money
through the grant funding system, which takes years and has a very high failure
rate. If funding is secured, various
causes of the disease would be suggested and tested by different investigating
teams. For an existing disease, existing hypotheses would likely be considered
and tested before GM foods are considered.
For example, an investigation into an increase in bowel cancer would
likely concentrate on the fat and fibre content of the food. Furthermore, obtaining accurate recall from
study subjects of foods that they may have eaten years ago is highly
inaccurate. Consumption of GM food components are even harder to quantify, as
many manufacturers still do not know whether they are using ingredients derived
from GM sources, or they do not label the food as containing these. This makes
it extremely difficult to determine the amount or types of GM foods eaten in a
group of ill people. It therefore becomes almost impossible to prove that a GM
food has caused a disease, even if there are thousands of cases. For these reasons, the OGTR’s assumption
that absence of evidence of harm is the same as evidence of absence of harm is
very dangerous.
Of
additional concern is that the OGTR is proposing minimal oversight conditions
on InVigor® canola that appear not to include any provisions for monitoring or
surveillance of InVigor® canola on human health. This is remarkable, as on the
one hand, the OGTR states that it will review the commercial release if there
is evidence of harm to human health.
However, it has then chosen a system of regulation that has excluded any
conditions or provisions that would determine if this harm was occurring. The
IHER regards this as negligent. An
active surveillance system is required.
There
appears to be no recall system in place if any adverse effect is found in the
environment or in animal or human health.
A comprehensive whole supply-chain recall system should be designed
before commercial release goes ahead, so that if any adverse effects are found,
an attempt can be made to remove the InVigor® canola from the environment.
In science,
results of new work are published in peer-reviewed scientific and medical
journals, so that others can repeat and extend the experiments and hence
build-up a picture-in-progress of the area.
This has not happened with InVigor® canola. This is of concern as a new concept or treatment in science often looks good
upon first report only to fall into disrepute after further investigation. Unfortunately, there are serious signs that
this may be the situation with InVigor® canola. One reason is that a
little investigation of the references (including who the authors work for or
were funded-by) cited by the OGTR shows that by far the greatest number of
experiments cited have been done by vested interests rather than independent
scientists. Moreover, much of their
work is in the form of internal company documents, a situation which prevents
peer review by experts in the field. Consequently, the accuracy and veracity of
the findings, and the methods employed have not come under scrutiny by other
scientists. In addition, little of
their work has been repeated by others to check the findings. There is also no
information about whether some of these documents were submitted to
peer-reviewed journals and were rejected.
Many reports are therefore unchecked, unverified (and possibly
peer-review rejected) experiments from Bayer and Monsanto.
Furthermore, the quality of the experimentation has
been very poor. Experiments have simply
not been designed to thoroughly investigate the possibility of harm from these
GM organisms to the environment, livestock or people. This may be why many of these studies were never submitted to
journals for peer-review. On the data
presented in the OGTR document, many simply would not meet the standards
required for submission. Another
concern is the clear conflict of interest in an applicant company doing its own
safety assessments. The company will
clearly benefit financially if the OGTR finds that InVigor® canola is safe for
health and the environment, yet the OGTR appear to be accepting their safety
evidence without discount and in the absence of much in the way of independent
assessments. Even worse, where an
alternative view exists, the OGTR dismisses it. In
addition, there are many claims made that are simply not backed-up by any
experimentation at all. For example,
because there have not been any experiments undertaken on ecological damage or
damage to health from InVigor® canola, the OGTR assumes that this absence of
evidence of harm is the same as evidence of absence of harm. The IHER contends that given the history of
science, the OGTR is stepping on very dangerous ground indeed.
The US Council of Sate Governments has identified
some of the most common indicators of poor or questionable science. These are (1) observer bias and vested
interest, (2) important variables that are either overlooked of ignored, (3)
inadequate sample size or biased sample collection, (4) conclusions based on personal
stories or anecdotal evidence, (5) correlation confused with cause and effect,
(6) statements of uncertainty, (7) lack of helpful standard of reference, and
(8) lack of peer review. On this basis,
the evidence used by the OGTR and its risk assessment and risk management plan
exhibit poor and questionable science.
Yet the OGTR seems to accept this evidence as if it
comes from unchallengeable references.
In contrast, the OGTR admits to very few alternative views or
experimental data, and when it does, it discounts them or views them as
“questioned” or “debated”. This even
occurred when the alternative data came from in vivo experiments against the OGTR’s preferred in vitro results for transfer of DNA
into tissues. The OGTR then
inexplicably preferred in vivo
results over in vitro results when
considering horizontal gene transfer to bacteria. That is, although horizontal gene transfer has been shown to
occur in vitro, it questioned the
relevance of these studies to in vivo
conditions.
Genetic engineering is a technology in its infancy. We know enough about the technology to make GE crops, but we don’t know enough about the technology to predict what the short and long-term consequences will be. For example, it has recently been determined that GM DNA can transfer into bacteria in the gut of people after just one meal containing GM soy. This was not supposed to happen. Under these conditions, it is wisest to use the Precautionary Principle, which acknowledges our ignorance about many aspects of the environment and human health. It has the underlying principle that a new organism should be treated as harmful until proven safe. It acknowledges scientific uncertainty and guides our actions in response to this uncertainty. The Precautionary Principle states that: “When an activity raises threats of harm to human health or the environment, precautionary measures should be taken even if some cause and effect relationships are not fully established scientifically. In this context, the proponent of the activity, rather than the public, should bear the burden of proof”. It also states that :