2014 A1094 Application FSANZ Cotton 29 April 2014

29 April 2014

Food Standards Australia New Zealand

WELLINGTON 6143 and CANBERRA BC ACT 2610

Application A1094 – Food derived from Herbicide-tolerant Cotton Line DAS-81910-7 – Dow AgroSciences Australia Limited – genetically engineered to provide tolerance to 2,4-D

(2,4-dichlorophenoxyacetic acid and glufosinate ammonium.

Taking into account the following material, the Trustees and Members of PSGR urge Food Standards Australia New Zealand (FSANZ) to reject this application.

1 – Transgenic foods and safety

Pharmaceuticals are distinct and identifiable single agents. A new pharmaceutical is not approved without extensive animal and human trials to demonstrate relative safety and define risks and benefits. Even then it is recognized a high percentage of side effects are not discovered until after the drug is released for general use. It is an acknowledged risk that a new pharmaceutical chemical given orally is a “prescription poison” and the recognized and unrecognized and the unintended effects of pharmaceuticals are assessed by the medical practitioner and the patient. A new pharmaceutical requires an individualised prescription from a registered medical doctor and potentially informed consent from patients. Post-marketing surveillance effectively extends indefinitely.

Foods derived using genetic engineering technology contain unpredictable changes in plant chemistry; multiple and complex alterations. They also retain higher residue levels of pesticides; sometimes multiple pesticides where gene stacking is applied. There is no justifiable scientific basis to claim any food plant with novel engineered DNA as “equivalent” to a conventional food plant.[i] By its very definition it is different. It is irresponsible to use such an unsubstantiated statement, especially by food regulators who have a clearly defined duty of care to uphold public safety and health under administrative law.

Studies to prove the safety claimed have simply not been carried out.[ii] Most studies to claim transgenic food crops to be safe are run for relatively short periods and largely conducted by the developer of the seed; a body that will benefit from sales of the product. This practice is inadequate, unacceptable and irresponsible. We refer you to the guidelines issued by the European Food Safety Authority for two-year whole food rodent feeding studies to assess the risks of long-term toxicity and the establishment of protocols for case-by-case studies.[iii] [iv] These at least are an improvement on current practices.

The inherent difference of transgenic foods from non-genetically engineered counterparts, and the attendant risk any difference creates to human health, dictates that foods containing novel DNA sequences should be regulated as if they were substantially equivalent to pharmaceuticals. This would include significant animal and human testing, and post-marketing surveillance on human health effects. It would also require informed consent from consumers.

This application to introduce food derived from such transgenic sources into the New Zealand food supply endangers every consumer, particularly our most vulnerable: pregnant women, their unborn children and infants and the elderly. As there is no expected health benefit to a transgenic food over a non-transgenic food medical ethics would require that a medical practitioner advise patients to avoid genetically engineered sourced foods.

Prior to their release, the consensus of scientists working at the US FDA was that transgenic foods were inherently dangerous, and might create hard-to-detect allergies, poisons, gene transfer to gut bacteria, new diseases, and nutritional problems. They urged rigorous long-term tests.[v] In a recent review of transgenic crops based on cultivation since 1996, the US Department of Agriculture said, “it is not clear that the first generation GE seeds will benefit farmers indefinitely.” It is certain they do not benefit consumers.[vi]

The 2014 ‘Hot Debate’ at Lincoln University featured six experts, including scientists from Crown Research Institutes. The panel were asked, as the scientists involved stated that GE foods were safe to eat, would they provide 10 human studies to back up their statements, and would they also advise where the diagnostic tools are available for health professionals to identify if GE food in the human diet may be contributing to illness? The panel members presenting proponents of genetic engineering - Dr Jon Hickford and Dr Tony Connor - admitted there are no studies or diagnostic tools for monitoring public health impacts of GE food.[vii] It is time this situation was remedied.

2 – Transgenic foods, pesticide-resistance and human health

Largely because of failures in crops resistant to glufosinate ammonium and other herbicides/pesticides, seed developers want approval for transgenic crops resistant to more toxic chemicals, including 2,4-D (2,4-Dichlorophenoxyacetic acid).

2,4-D is linked to liver damage, endocrine disruption, depressed thyroid hormone levels, infertility and cancer. See also Addendum A.

Glufosinate ammonium inhibits the enzyme glutamine synthetase, necessary for the production of glutamine and for ammonia detoxification. It inhibits the same enzyme in animals.

Transgenes express in the xylem of plants: leaves, fruit, flowers, pollen, nectar, and guttation fluid of plants. Whatever part of a transgenic plant is used as a food or food ingredient, the consumer will ingest transgenes. Consumers will also ingest increased residues from chemical sprays.

Animals fed transgenes have responded with a wide variety of health problems. This suggests people will also react to ingesting transgenic food/s with multiple symptoms. Indicative of this could be the fact that in the first nine years following commercial introduction of transgenic crops in 1996, the incidence of US citizens with three or more chronic diseases nearly doubled; 7% to 13%.[viii]

Statistics show pesticides use in the US has almost doubled since the introduction of genetically engineered crops grown commercially. Farmers are spraying more simply because they can without harming their herbicide-resistant crops. This process of over spraying leaves standing crops contaminated with increased residual spray and these same plants then grow in ground retaining above-the-norm residues of the chemical spray/s, residues which they can uptake.

Desiccation, spraying close to harvest to suggest uniform maturity and facilitate easy lifting of the yield, also leaves significant residual chemical/s on the crops close to harvesting. MAFF UK states that when used as a desiccant, glufosinate residues are detectable in dried peas, field beans, wheat, barley, oilseed rape, and linseed; all of which can be used as food or feed ingredients. Wheat grain containing residues ground into flour retained 10-100% of the residue; bran residue levels 10-600% of those in grain.[ix] Such residues or a significant portion would be ingested.

The cumulative effects of ingesting growing quantities of multiple and substantially different sequences of novel DNA on a daily basis, potentially for a lifetime has not been pursued officially. Effectively, populations, especially in the US, have unknowingly acted as guinea pigs for an ongoing experiment that no official body is monitoring or evaluating.

Animal studies indicate there will be adverse effects from ingesting transgenic foods and professional bodies point to the evidence accumulating that consuming genetically engineered foods has adverse effects on human health. [x] [xi] [xii] [xiii] Medical professionals and veterinarians in the US are advising patients, pet owners and farmers not to eat transgenic foods or feed them to pets or livestock. The results reported are substantial improvements in health and well-being.

In 2011, 90 percent of the US cotton crop was transgenic,[xiv] a statistic which suggests 90 percent of ingested food products containing cottonseed derivatives can potentially contain transgenic DNA. Where it was assumed 50% of the diet came from transgenic foods and transgenes represent an estimated 0.0005% of the total DNA in food, one study put the consumption figure at 0.5–5 μg/day. While DNA is claimed as mostly degraded during the industrial process and in the digestive tract, fragments have been detected in body tissues such as leukocytes, liver, spleen and gut bacteria[xv]. Fragments of orally administered phage M13 and plant DNA were taken up by phagocytes as part of their normal function as immune system cells.[xvi] Fragments could pass into other organs, including a foetus.[xvii]

A 2010 study found pesticide exposure in general resulted in reduced fertility in males, genetic alterations in sperm, a reduced number of sperm, damage to germinal epithelium and altered hormone function.[xviii] A further study found significant associations between impaired semen parameters and 2,4-D.[xix] [xx] [xxi] Some of the potential reproductive health effects of pesticides include reduced fertility, early and late pregnancy loss, premature birth and reproductive system effects, reduced fertility, genetic alterations in sperm, reduced number of sperm, damage to germinal epithelium, altered hormone function, low birth weight/small for gestational age and developmental defects.[xxii] [xxiii]

In food crops developed to resist 2,4-D and glufosinate ammonium consumers will, without knowing, be ingesting the resistant transgene/s, even if as minute fragments, from whatever part of the plant they consume. They will also ingest residues of liberal herbicide applications.[xxiv] Agricultural sprays also include adjuvants and surfactants, which ingredients are frequently more toxic than the pesticide itself.[xxv]

In a study published in December 2013, researchers tested the toxicity of nine pesticides involving the active ingredient and the added ingredients. Their results “challenge the relevance of the Acceptable Daily Intake for pesticides because this norm is calculated from the toxicity of the active principle alone. ... Chronic tests on pesticides may not reflect relevant environmental exposures if only one ingredient of these mixtures is tested alone.”[xxvi][xxvii] [xxviii]

Official bodies accepting the word of developers, and vested interests continuing to deny the possibility of adverse effects, does not mean there are none.[xxix] Animal studies reveal the potential for conditions presenting now and in the short- and long-term future. One suggested exposure to even low doses of glufosinate in the infantile period in rats causes changes in the kainic acid receptor in the brain.[xxx] In another study, mouse embryos exposed to glufosinate in vitro developed apoptosis (fragmentation of the cells leading to cell death) in the neuroepithelium of the brain.[xxxi] An earlier study found all embryos in treated groups had specific defects including overall growth retardation, increased death of embryos, hypoplasia (incomplete g/ml, and cleft lips at 20μ development) of the forebrain at 10g/ml.[xxxii]

There is support for the specificity of the association of transgenic foods and specific disease processes. Multiple animal studies show significant immune dysregulation, including upregulation of cytokines associated with asthma, allergy, and inflammation.[xxxiii]

The American Academy of Environmental Medicine[xxxiv] has stated, “GM foods pose a serious health risk in the areas of toxicology, allergy and immune function, reproductive health, and metabolic, physiologic and genetic health and are without benefit. There is more than a casual association between GM foods and adverse health effects. There is causation as defined by Hill's Criteria[xxxv] in the areas of strength of association, consistency, specificity, biological gradient and biological plausibility. The strength of association and consistency between GM foods and disease is confirmed in several animal studies.”

AAEM states, "Multiple animal studies show significant immune dysregulation," including increase in cytokines, which are "associated with asthma, allergy, and inflammation"—all on the rise in the US. The Academy says animal studies also show altered structure and function of the liver, including altered lipid and carbohydrate metabolism as well as cellular changes that could lead to accelerated aging and possibly lead to the accumulation of reactive oxygen species (ROS).[xxxvi] Changes in the kidney, pancreas and spleen have been documented.[xxxvii]

Ingested transgenic DNA does transfer to gut bacteria. Studies found intestinal damage in animals fed transgenic foods, including proliferative cell growth[xxxviii] and disruption of the intestinal immune system.[xxxix] In 2004, it was proven transgenes move from ingested food to bacteria in the human gut.[xl] An earlier, four-year study, found the transgene conferring resistance to glufosinate had transferred in bees’ guts to microbes.[xli] Since the pat gene can transfer to gut bacteria in bees, and since genetic material from transgenic soy can transfer to human gut bacteria, the pat gene can potentially transfer from any transgene to human intestinal flora.

There is also an absence of substantive data on the potential interactions of chemicals that a transgenic product has been designed to resist and an absence of data to assess potential health risks to humans through unique combinations of chemicals in food that are accepted as probable or feasible. This is an unmanaged risk.

It is crucial to prevent the foregoing risks becoming reality in the interests of public health, and to meet FSANZ’s mandated duty of care. The cost to the Health System of ignoring risks could be huge.

Equally, without comprehensive labelling, consumers will not know they are ingesting resistant transgene/s, even if as minute fragments. They will also be exposed to residues of greater than average herbicide applications, and be exposed to the spray regime associated with plant desiccation prior to harvest. All this is without monitoring of health effects or independent studies.

PSGR urges FSANZ to curb the risks now.

Uphold public safety by banning transgenic foods from the New Zealand food supply, as there is no scientific proof that they are equivalent to non-transgenic foods or that they are safe.

If transgenic foods continue to be allowed into the New Zealand food supply FSANZ should insist on comprehensive mandatory labelling to identify them, to warn of potential health risks, and to give consumers a choice.

The Trustees and Members of Physicians and Scientists for Global Responsibility

Addendum A

Extracts from ‘Overview of the toxic effects of 2,4-D’

Sierra Club of Canada

“there is a large body of evidence indicating major health effects, from cancer to immune-suppression, reproductive damage to neurotoxicity.”

In mammals, 2,4-D “disrupts energy production (Zychlinkski & Zolnierowicz, 1990), depleting the body of its primary energy molecule, ATP (adenosine triphosphate) (Palmiera et al., 1994). 2,4-D has been shown to cause cellular mutations which can lead to cancer.” This mutagen contains dioxins, a group of chemicals known to be hazardous to human health and to the environment (Littorin, 1994).

“Numerous epidemiological studies have linked 2,4-D to non-Hodgkin’s lymphoma (NHL) among farmers (Zahm, 1997; Fontana et al, 1998, Zahm & Blair, 1992, Morrison et al. 1992).

“Multi-center studies in Canada and in Sweden of members of the general public found a 30-50% higher odds of 2,4-D exposure among people with NHL(McDuffie et al. 2001, Hardell & Eriksson, 1999, Sterling & Arundel, 1986).

“The teratogenic, neurotoxic, immunosuppressive, cytotoxic and hepatoxic effects of 2,4-D have been well documented (Blakely et al., 1989; Sulik et al, 1998; Barnekow et al., 2000; Rosso et al., 2000; Venkov et al., 2000; Charles et al., 2001; Madrigal-Bujadar et al., 2001; Osaki et al., 2001; Tuschl & Schwab, 2003).

“Other researchers publishing in the open scientific literature have reported oxidant effects of 2,4-D, indicating the potential for cytotoxicity or genotoxicity. For example, Bukowska (2003) reported that treatment of human erythrocytes in vitro with 2,4-D at 250 and 500 ppm resulted in decreased levels of reduced glutathione, decreased activity of superoxide dismutase, and increased levels of glutathione peroxidase. These significant changes in antioxidant enzyme activities and evidence of oxidative stress indicate that 2,4-D should be taken seriously as a cytotoxic and potentially genotoxic agent.”

It continues: “2,4-D causes significant suppression of thyroid hormone levels in ewes dosed with this chemical (Rawlings et al., 1998). Similar findings have been reported in rodents, with suppression of thyroid hormone levels, increases in thyroid gland weight, and decreases in weight of the ovaries and testes (Charles et al., 1996). The increases in thyroid gland weight are consistent with the suppression of thyroid hormones, since the gland generally hypertrophies in an attempt to compensate for insufficient circulating levels of thyroid hormones. Thyroid hormone is known to play a critical role in the development of the brain. Slight thyroid suppression has been shown to adversely affect neurological development in the foetus, resulting in lasting effects on child learning and behaviour (Haddow et al., 1999).

“2,4-D causes slight decreases in testosterone release and significant increases in estrogen release from testicular cells (Liu et al, 1996). In rodents, this chemical also increases levels of the hormones progesterone and prolactin, and causes abnormalities in the estrus cycle (Duffard et al, 1995).

“Male farm sprayers exposed to 2,4-D had lower sperm counts and more spermatic abnormalities compared to men who were not exposed to this chemical (Lerda & Rizzi, 1991).

In Minnesota, higher rates of birth defects have been observed in areas of the state with the highest use of 2,4-D and other herbicides of the same class. This increase in birth defects was most pronounced among infants who were conceived in the spring, the time of greatest herbicide use (Garry et al, 1996).

“2,4-D also interferes with the neurotransmitters serotonin and dopamine. In young organisms, exposure to 2,4-D results in delays in brain development and abnormal behaviour patterns, including apathy, decreased social interactions, repetitive movements, tremor, and immobility (Evangelista de Duffard et al, 1995). Females are more severely affected than males. Rodent studies have revealed a region-specific neurotoxic effect on the basal ganglia of the brain, resulting in an array of effects on critical neurotransmitters and adverse effects on behaviour (Bortolozzi et al., 2001).

“A peer-reviewed, developmental neurotoxicity study demonstrated severe neurotoxicity in young rats exposed to 2,4-D from postnatal days 12 to 25 at doses of 70 mg/kg/day. These pups showed decreases in GM1 level, diminution in myelin deposition and alterations in all behavioural tests at all doses (Rosso et al, 2000). This herbicide specifically appears to impair normal deposition of myelin in the developing brain (Duffard et al., 1996). The neurotoxic and anti thyroid effects of 2,4-D make it highly likely that foetuses, infants, and children will be more susceptible to long-term adverse health effects from exposure to this chemical although they may appear normal at birth.

Young animals can also be exposed to 2,4-D through maternal milk. Recent research has revealed that 2,4-D is excreted in breast milk, thereby resulting in potentially significant exposures to the nursling. The researchers detected 2,4-D residues in stomach content, blood, brain and kidney of 4-day-old neonates fed by 2,4-D exposed mothers (Sturtz et al., 2000). When maternal exposures stopped, the chemical continued to be excreted in maternal milk for a week. Thus, postnatal exposures to this chemical during the critical period for development of the infant brain are of serious scientific concern.”

Sierra Club of Canada

http://www.sierraclub.ca/national/programs/health-environment/pesticides/2-4-D-overview.pdf

[i] WHO answers questions on genetically modified foods http://www.who.int/mediacentre/news/notes/np5/en/

[ii] José Domingo, "Toxicity Studies of Genetically Modified Plants : A Review of the Published Literature," Critical reviews in food science and nutrition, 2007, vol. 47, no8, pp. 721-733

[iii] http://www.efsa.europa.eu/en/efsajournal/pub/3347.htm

[iv] EFSA Journal 2013;11(7):3347 [18 pp.]. doi:10.2903/j.efsa.2013.3347, European Food Safety Authority Acknowledgment Contact, Type: Scientific Report of EFSA On request from: European Commission Question number: EFSA-Q-2013-00316 Approved: 26 July 2013 Published: 31 July 2013 Affiliation: European Food Safety Authority (EFSA) Parma Italy, http://www.efsa.europa.eu/en/efsajournal/pub/3347.htm.

[v] [27] From information released by the Alliance for Bio-integrity http://www.biointegrity.org/

http://www.responsibletechnology.org/doctors-warn

[vi] http://www.i-sis.org.uk/Global_Status_of_GM_and_nonGMs.php

[vii] Myths Revealed About Safety of Genetically Engineered Food, GE Fee NZ Press Release 3 April 2014.

[viii] [30] Kathryn Anne Paez, et al, "Rising Out-Of-Pocket Spending For Chronic Conditions: A Ten-Year Trend," Health Affairs, 28, no. 1 (2009): 15-25

[ix] http://www.pan-uk.org/pestnews/Actives/glufosin.htm. Pers. Comm., MAFF, Pesticides Usage Survey Group. MAFF, York.

Agrow No. 273 January 31st 1997, p. 21; Watkins, 1995. MAFF, Evaluation No. 33 : HOE 399866 (Glufosinate-ammonium), Ministry of Agriculture Fisheries and Food, London, 1990. US EPA, Office of Pesticides and Toxic Substances, Experimental Use permit (6340-EUP-RN) and Temporary Tolerance Petition (4G3156) for HOE 39866. Memo from D.S. Saunders to R. Mountfort, Registration Division, 18th April 1985. MAFF, Health and Safety Executive,

1991. Advisory Committee on Pesticides Annual Report 1991, HMSO, London Fujii et al 1996; Watanabe, 1997; Watanabe and Iwasi, 1996. MAFF, Health and Safety Executive, 1991. Advisory Committee on Pesticides Annual Report 1991, HMSO, London; Pesticides Trust [now PAN UK], Crops Resistant to Glutamine Synthetase Inhibitors.

[x] ‘Experimental Evidence of GMO Hazards,’ Irina Ermakova, Presentation at Scientists for a GM Free Europe, EU Parliament, Brussels, June 12, 2007.

[xi] ‘Ultrastructural Analysis of Testes from Mice Fed on Genetically Modified Soybean’, L. Vecchio et al, European Journal of Histochemistry 48, no. 4 (Oct–Dec 2004):449–454.

[xii] ‘Temporary Depression of Transcription in Mouse Pre-implantion Embryos from Mice Fed on Genetically Modified Soybean,’ Oliveri et al., 48th Symposium of the Society for Histochemistry, Lake Maggiore (Italy), September 7–10, 2006.

[xiii] ‘Biological effects of transgenic maize NK603xMON810 fed in long term reproduction studies in mice,’ Velimirov and Binter, Forschungsberichte der Sektion IV, Band 3/2008.

[xiv] http://www.greenamerica.org/pubs/greenamerican/articles/AprilMay2012/9-GM-ingredients-to-watch.cfm

[xv] Schubbert et al., 1997

[xvi] Schubbert et al., 1998

[xvii] Beever et al., 2000; Goldstein et al., 2005; Jonas et al., 2001

[xviii] Environmental Impacts on Reproductive Health, (pub. January 2010), http://www.arhp.org/publications-and-resources/clinical-proceedings/RHE/Pesticides

[xix] Sheiner EK, Sheiner E, Hammel RD, Potashnik G, Carel R (April 2003). "Effect of occupational exposures on male fertility: literature review". Ind Health 41 (2): 55–62. doi:10.2486/indhealth.41.55. PMID 12725464. http://www.ncbi.nlm.nih.gov/pubmed/12725464

[xx] Environmental Protection Agency. Pesticides. Available at: http://www.epa.gov/pesticides. Accessed November 15, 2008.

[xxi] National Pesticide Information Center. http://npic.orst.edu/index.html. Accessed November 15, 2008.

[xxii] Figà-Talamanca I, Traina ME, Urbani E. Occupational exposures to metals, solvents, and pesticides: recent evidence on male reproductive effects and biological markers. Occup Med. 2001;51(3):174–88.

Whorton MD, Krauss RM, Marshall S, Milby TH. Infertility in male pesticide workers. Lancet. 1977;2:1259–61.

[xxiii] Bretveld RW, Thomas CMG, Scheepers PTJ, et al. Pesticide exposure: the hormonal function of the female reproductive system disrupted? Reprod Biol Endocrinol. 2006;4:30.

[xxiv] http://www.ifrc.org/PageFiles/89755/Photos/307000-WDR-2011-FINAL-email-1.pdf.

www.gmo-compass.org/eng/agri_biotechnology/gmo_planting/257.global_gm_planting_2009.html.

[xxv] ‘Glyphosate commercial formulation causes cytotoxicity, oxidative effects, and apoptosis on human cells: differences with its active ingredient’, Chaufan et al, Int J Toxicol. 2014, 16 January 2014, PMID: 24434723 http://www.ncbi.nlm.nih.gov/pubmed/24434723?dopt=Abstract

[xxvi] ‘Major pesticides are more toxic to human cells than their declared active principles’, Mesnage et al, http://www.hindawi.com/journals/bmri/aip/179691/

[xxvii] http://www.panap.net/sites/default/files/monograph_glyphosate.pdf

[xxviii] Mesnage R, Defarge N, Spiroux de Vendômois J, Séralini G-E. Major pesticides are more toxic to human cells than their declared active principles. Biomedical Research International, 2014. http://www.hindawi.com/journals/bmri/aip/179691/

[xxix] The US Environmental Protection Agency on 2,4-D www.epa.gov/oppsrrd1/REDs/factsheets/24d_fs.htm.

[xxx] Fujii, T., T. Ohata, M. Horinaka, Alternations in the response to kainic acid in rats exposed to glufosinate-ammonium, a herbicide, during infantile period. Proc. Of the Japan Acad. Series B-Physical and Biological Sciences, 1996, Vol. 72, No. 1, pp. 7-10.

[xxxi] Watanabe, T. , Apoptosis induced by glufosinate ammonium in the neuroepithelium of developing mouse embryos in culture. Neuroscientific Letters, 1997, Vol. 222, No. 1, pp.17-20. 17.

[xxxii] Watanabe, T. and T. Iwase, Development and dymorphogenic effects of glufosinate ammonium on mouse embryos in culture. Teratogenesis carcinogenesis and mutagenesis, 1996, Vol. 16, No. 6, pp. 287-299.

[xxxiii] Finamore A, Roselli M, Britti S, et al. Intestinal and peripheral immune response to MON 810 maize ingestion in weaning and old mice. J Agric. Food Chem. 2008; 56(23):11533-11539. Kroghsbo S, Madsen C, Poulsen M, et al. Immunotoxicological studies of genetically modified rice expression PHA-E lectin or Bt toxin in Wistar rats. Toxicology. 2008; 245:24-34.

[xxxiv] http://www.aaemonline.org/gmopost.html.

[xxxv] Hill, AB. The environment and disease: association or causation? Proceeding of the Royal Society of Medicine 1965; 58:295-300.

[xxxvi] Malatesta M, Boraldi F, Annovi G, et al. A long-term study on female mice fed on a genetically modified soybean:effects on liver ageing. Histochem Cell Biol. 2008; 130:967-977. Velimirov A, Binter C, Zentek J. Biological effects of transgenic maize NK603xMON810 fed in long term reproduction studies in mice. Report-Federal Ministry of Health, Family and Youth. 2008.

Kilic A, Aday M. A three generational study with genetically modified Bt corn in rats: biochemical and histopathological investigation. Food Chem. Toxicol. 2008; 46(3):1164-11707

[xxxvii] Finamore A, Roselli M, Britti S, et al. Intestinal and peripheral immune response to MON 810 maize ingestion in weaning and old mice. J Agric. Food Chem. 2008; 56(23):11533-11539. Velimirov A, Binter C, Zentek J. Biological effects of transgenic maize NK603xMON810 fed in long term reproduction studies in mice. Report-Federal Ministry of Health, Family and Youth. 2008.

Kilic A, Aday M. A three generational study with genetically modified Bt corn in rats: biochemical and histopathological investigation. Food Chem. Toxicol. 2008; 46(3):1164-1170.

[xxxviii] Ewen S, Pustzai A. Effects of diets containing genetically modified potatoes expressing Galanthus nivalis lectin on rat small intestine.Lancet. 354:1353-1354.

[xxxix] Finamore A, Roselli M, Britti S, et al. Intestinal and peripheral immune response to MON 810 maize ingestion in weaning and old mice. J Agric. Food Chem. 2008; 56(23):11533-11539.

[xl] ‘Assessing the survival of transgenic plant DNA in the human gastrointestinal tract’, Netherwood et al., Nat Biotechnol. 2004 Feb;22(2):204-9. Epub 2004 Jan 18.http://www.ncbi.nlm.nih.gov/pubmed/14730317.

[xli] Antony Barnett, New Research Shows Genetically Modified Genes Are Jumping Species Barrier, London Observer, May 28, 2000. Research carried out by Professor Dr Han-Hinrich Kaatz, when Head of Apidology at the Institute for Bee Research, University of Jena.

Ends