9 Contested Viewpoints on the Health Effects of GMOs
Thus far, I have explored the mainstream scientific literature on the principles of traditional and molecular breeding, pointing out where there are contested viewpoints. I have discussed how the methods of breeding may introduce unintended effects and questioned whether molecular breeding introduces any unique health or environmental impacts from the crops produced and foods derived from them. Looking into competing scientific interpretations may help to explain why there are wide divisions in society over GMOs. It is too easy to say that one group follows the science and the other group follows an ideology. That leads some observers to embrace the idea of “GMO deniers,” referring to people who leave the science behind in favor of an irrational (or groundless) opposition to genetically modified food. But there is a scientific record of studies that support honest skepticism. Also, European and American scientists see the issues and the risks differently, which can explain why their respective regulatory systems are distinct.
In this chapter, I explore contested principles held by scientists that reflect not so much different interpretations of the same science but rather alternative presuppositions about how to apply the knowledge of plant genetics to the questions of risk and why scientists may reach different conclusions. There is a great deal that plant biologists agree upon, which is covered in the previous chapters. Here I focus on principles or conclusions for which there is lack of consensus—at least among certain groups of scientists. By focusing on the contested interpretations of general principles, I will be able to highlight the locus of disagreement.
Contested Point 1: Traditional and Molecular Breeding Are (Are Not) Qualitatively Distinct.
The mainstream position—based on reports of the National Academies of Sciences, Engineering, and Medicine (NASEM), government agencies, and professional agricultural organizations in plant breeding—is that different forms of breeding may produce unpredictable and unexpected effects and that there is nothing inherently riskier about molecular breeding using genetic engineering than breeding involving wide crosses, embryo rescue, or induced mutations. As Andrew Cockburn notes, “enormous random changes can result from chemical and irradiation mutagenesis, which is also traditionally used for crop breeding.”1 As already mentioned, there is no database of breeding methods that compiles adverse, unintended effects. In both traditional and molecular breeding, there is a considerable knowledge gap.
Skeptics of the mainstream position claim that molecular breeding presents unique risks because it bypasses the plant’s natural gene regulation system and reprograms part of the genetic functions of the plant genome. In contrast, natural breeding uses the genes in the plants or in closely related plants and does not involve introducing foreign markers and promoter genes into a host plant genome. The skeptics acknowledge that there are risks of mutational breeding, which induces DNA mutations in plant cells (genome) by radiation or chemicals. But with mutagenesis, the germ plasm of the plant is the starting material. You can only go so far in creating mutations in the existing DNA of a plant. In molecular breeding, the scientist creates a gene cassette made up of a foreign promoter gene—the gene from another species and possibly kingdom that provides the plant with a qualitatively new phenotype (insect resistance), a marker gene, and a terminator gene that tells the cell when to stop transcription (when to stop the reading frame). Each of these components comes potentially from a different source that is not available to a traditional breeder.
There are also cases where molecular breeders use promoters from the parental crop or from sexually compatible plants and remove the marker genes before entering the market. A genetically engineered potato was made using genetic components from wild relatives. The genetically modified Innate potato, developed by the J. R. Simplot Company, was approved by the U.S. Department of Agriculture (USDA) in 2014 and the Federal Drug Administration (FDA) in 2015. Innate was designed with lower amounts of the amino acid asparagine, which turns into acrylamide (a toxin) during frying. It does not contain genetic components from other species.2
Some commentators compare radiation-induced mutagenesis with molecular breeding, arguing that since the former is considered part of conventional breeding, and it is unregulated and unpredictable, then molecular breeding also should be unregulated. GMO skeptics like John Fagan, Michael Antoniou, and Claire Robinson argue that “Comparing genetic engineering with radiation-induced mutagenesis and concluding it is safe is like comparing a game of Russian Roulette played with one type of gun with a game of Russian Roulette played with another type of gun. Neither is safe.”3
According to the Council of Europe in 1990, GMOs are “organisms in which the genetic material has been altered in a way that does not occur naturally by mating or natural recombination.”4 The Council excludes from its meaning of GMO (what I have termed molecular breeding) mutagenesis, cell fusion, and protoplast fusion, which they classify under traditional breeding methods. The chemical mutagenesis and radiation mutagenesis of plants affect genes, so they can fit under the strict definition of molecular breeding. However, they remain part of traditional breeding both in Europe and the United States because they do not use in vitro methods of cutting and splicing genes.
Contested Point 2: Molecular Breeding Is (Is Not) More Precise Than Traditional Breeding and Consequently Safer (Not Safer).
It is often argued that GMOs are the result of methods that use greater precision than those of traditional breeding techniques in creating genetic changes in plant species. In some respects, this is correct. Plant scientists can isolate a gene and create a specific gene cassette that is transferred to plant cells. In other forms of breeding, getting the right genes into the target cultivar is a trial and error process, and the breeding process combines more than the genes responsible for the traits.
GMO skeptics argue that precision is more than isolating a gene for transfer into plant cells. Precision also involves achieving a desired outcome from the transfer of the gene cassette into the parental plant. It is generally agreed that the gene cassette, which is introduced into plant cells by either Agrobacterium tumefaciens or biolistics, is randomly placed in the chromosome.5 The precision of the gene splicing is turned into imprecision when the gene cassette gets inserted into plant cells. The position effect (the variation of expression exhibited by identical transgenes that are inserted into different regions of a genome) on plant phenotypes is a well-recognized phenomenon. For GMO skeptics, it means uncertain risks. For GMO promoters, it means that breeders can select against any adverse pleotropic effects (the effects from one gene influencing two or more other phenotypic traits). Not only is there imprecision in the location of the transgene, but there is also uncertainty about whether the promoters in the gene cassette will affect other genes near or around the cassette.
In their analysis of transgenic insertions, Johnathan R. Lathan, Allison K. Wilson, and Ricarda A. Steinbrecher write: “Despite the supposed precision of genetic engineering, it is common knowledge that large numbers of individual transgenic plants must be produced in order to obtain one or a few plants that express the desired trait in an otherwise normal plant.”6 Others, like Nina Federoff and Nancy Marie Brown, are more optimistic about the plant’s ability to accommodate to insertion mutagenesis or other perturbations in the plant genome: “A gene’s location, while not unimportant, is less important than what the gene is and what it codes for.”7 Although the position effect is generally accepted, advocates for not treating molecular breeding as unique say that experience allows the plant breeders to select healthy plantlets with the desired traits. The GMO skeptics recoil at relying on this confidence in the breeders: “Even after selection, there are many reports of apparently normal transgenic plants exhibiting aberrant behavioural or biochemical characteristic upon further analysis.”8 H. A. Kuiper, G. A. Kleter, P. Hub, J. M. Noteborn, and E. J. Ko have documented a number of unintended effects in genetically engineered crops.9
Federoff and Brown believe that these aberrant effects will be picked up by the breeders’ discretion before the crops are marketed: “And if an insertion is bad for the plant, the contemporary breeder does precisely what [Luther] Burbank did—throws the plant out. But modern breeders … can analyze the proteins, nucleic acids, fats and starches, as well as all of the many molecules (called secondary metabolites) that the genetically modified plant makes. They can compare this analysis to the chemical profile of the variety from which the plant was derived and ask, is this the same plant, except for that one protein encoded by the added gene.”10
The question remains, Will the breeders perform the functions outlined by Federoff and Brown? And will an unanticipated adverse effect manifest itself right away or gradually over a period of consumption years? In the former case, stalwart GMO promoters argue that the time, effort, and cost of identifying adverse effects before commercialization are not justified, whereas GMO skeptics are faithful to the precautionary principle. In the latter case, how many years will it take for the adverse effect to show up after the product is approved and placed on the market? Can the adverse effect be picked up by premarket testing through compositional analysis or animal feeding studies?
Contested Point 3: The Concept of Substantial Equivalence Is (Is Not) an Effective Sorting Method for Determining Which Transgenic Plants Need Greater Regulatory Oversight.
The concept of substantial equivalence was created with two points in mind. First, it serves as a standard for sorting the products of molecular breeding into those that should and those that should not require greater regulatory oversight and risk assessment beyond what is required of the non-GM parental strain or any conventionally bred counterpart. Second, it was thought of as a starting point in risk assessment “that provides guidance by helping to identify questions to be asked during the safety assessment.”11
The concept was first introduced by a panel of scientists who were assigned to develop safety criteria for foods and crops that were developed through biotechnology under the auspices of the Organisation for Economic Co-operation and Development (OECD), an intergovernmental economic organization. The panel’s report, titled Agricultural Policies in OECD Countries: Monitoring and Evaluation 2000, discusses “substantial equivalence” for new foods or food components derived by modern biotechnology.12 According to the panel’s viewpoint, a transgenic crop can be compared to a parental (or conventionally bred counterpart) crop from which it was derived, about which there is extensive knowledge of possible toxicants, critical nutrients, and other relevant characteristics. When extensively analyzed, if the transgenic crop exhibits no significant changes in its components or traits compared to the parental strain (or conventionally bred counterpart), it can be treated as “substantially equivalent” to that strain. After that determination is made, further safety or nutritional concerns are expected to be insignificant. Food that is found to be substantially equivalent to a parental strain can be treated, for food safety purposes, in the same manner as its conventional counterparts.
In U.S. policy, the finding of substantial equivalence for a transgenic crop is analogous to the designation of generally regarded as safe (GRAS) for food additives. According to biotechnology promoters, the value of this category is that it prevents redundant testing and regulatory burden on producers. Unlike European policy, a GRAS finding in the U.S. policy is attributed to all GMOs prior to testing.
GMO skeptics deride the concept of substantial equivalence as vague and prone to regulatory discretion and producer lobbying because there are no canonical tests that establish equivalence in nutrients and traits. As Erik Millstone, Eric Brunner, and Sue Mayer write in Nature: “The concept of substantial equivalence has never been properly defined; the degree of difference between a natural food and its GM alternative before its ‘substance’ ceases to be acceptably ‘equivalent’ is not defined anywhere.… Substantial equivalence is a pseudo-scientific concept because it is a commercial and political judgment masquerading as if it were scientific … created primarily to provide an excuse for not requiring biochemical or toxicological tests.”13 Cockburn, a Monsanto scientist, disputes Millstone and his colleagues in a single sentence: “This argument which aligns with the inability to prove a negative is equally applicable to so-called conventionally bred crops and is therefore disproportionate and specious: it makes no sense to single out GM crops.”14 However, after the fact that traditional breeding and molecular breeding are distinct is accepted, then the concept of whether “substantial equivalence” is properly defined can be discussed.
What evidence is there that GMOs, which were designated as substantially equivalent, have nutritional and toxicological profiles that are not significantly different than that of the parental strains or a conventionally bred counterpart? Fagan, Antoniou, and Robinson report a number of cases where significant differences were found: “Commercialized MON810 GM maize had a markedly different profile in the types of proteins it contained compared with the non-GM counterpart when grown under the same conditions. These unexpected compositional differences also showed that the MON810 maize was not substantially equivalent to the non-GM isogenic comparator even though worldwide regulatory approvals of this maize had assumed that it was.”15 It is possible that many approved transgenic crops are not substantially similar to the non-GMO parental strain or a conventionally bred counterpart, but that does not mean they are unsafe to eat or unhealthy for the environment. The sorting criteria, the risk assessment, and the tested effects of GMOs on human consumers are all distinct issues that can be evaluated on different empirical evidence.
Contested Point 4: A Transgene That Is Used to Alter a Biochemical Pathway in a Plant, That Alters a Protein Synthesis, and That Is Not Found in Humans Is (or Is Not) Inherently Safe for Humans.
Some plant geneticists have stated that herbicides or pesticides that interact with a plant’s enzyme systems and result in plant death do not affect humans who lack the same enzyme pathway. Thus, the herbicide glyphosate kills plants by interfering with the enzyme excitatory postsynaptic potential (EPSP) synthase that is essential for synthesizing certain essential amino acids (the aromatic amino acids phenylalanine, tyrosine, and tryptophan). Paul Lurquin writes that “humans do not possess the EPSP synthase, the enzyme, and as a result, our protein synthesis mechanism cannot be inhibited by glyphosate.”16 Monsanto advertises that Roundup is safe for humans and pets because it targets an enzyme that is not present in humans or pets. Athenex Corporation submitted a toxicological review to the FDA of a glyphosate tolerant enzyme (EPSPS) on behalf of a commercial sponsor: “Because the shikimate pathway [a seven-step metabolic route that is used by bacteria, fungi, algae, parasites, and plants for the biosynthesis of aromatic amino acids (phenylalanine, tyrosine, and tryptophan)] is not present in animals, glyphosate has a favorable toxicology profile and has become a very common non-selective herbicide.”17 A similar conclusion was drawn by Lurquin in his book High Tech Harvest: Understanding Genetically Modified Food Plants about a pathway for making plants tolerant to the herbicide glufosinate: “Glufosinate is safe for humans because we do not convert nitrate into ammonia and do not use ammonia to make the amino acid glutamine,” and because other animals do not use ammonia to make glutamine, glufosinate is not harmful to them.18
But this leaves the question open: Can a chemical affect different pathways in plants and animals? When studying the toxicology of chemicals, carcinogenicity, genotoxicity (mutagenicity), allergenicity, endocrine disruption, and neurotoxicity must be considered. Each of these outcomes has a different pathway of action. If a chemical can have multiple endpoints of activity, why should we expect that it operates only within a single chemical pathway? This raises an important question: because we cannot know in advance how many pathways a chemical can use, how can we exercise a satisfactory risk assessment of the chemical in a new biological environment?
Cockburn addresses the issue of when a modified gene leads to a changed metabolic pathway or a new biochemical pathway. He proposes a “full analysis of the gene for open reading frames, ribosome binding sites.… Moreover, the metabolic economy of the cell may be altered upstream or downstream of the targeted change in the pathway affecting the overall nutritional and or toxicological profile of the crop.”19 This point about unanticipated metabolic pathways in GMOs was not made by a GMO skeptic but rather by a scientist at Monsanto. The issue has to be addressed by testing and not by assuming the transgenic crop is GRAS. Thus, glyphosate should not be assumed to disrupt only an enzyme pathway in plants that is not found in humans. But unless that is the only pathway with which it can interact, its other potential effects cannot be assumed not to exist.
These concerns about alternative pathways are illustrated in a 2018 study conducted by the Ramazzini Institute of Italy. Researchers fed levels of glyphosate, considered safe under U.S. standards, to rats and found that the glyphosate-fed rat pups had significant alterations in their microbiome compared to controls. This is an example of another pathway to illness through alteration of the microbiome. The authors conclude, “these data strongly indicate that GBHs [glyphosate-based herbicides] can exert long-lasting health effects later in life.”20
Contested Point 5: GMOs Have (Have Not) Been Adequately Evaluated for Health Effects.
The scientists who have confidence in the safety of GMOs for human consumption support their claims with specific evidence or background information. A summary of these arguments follows. First, GMOs have been rigorously tested by companies and overseen by agencies to ensure their safety. These claims have been echoed in the scientific literature. For example, Suzie Key, Julian K.-C. Ma, and Pascal M. W. Drake write in the Journal of the Royal Society of Medicine that “GM plants undergo extensive safety testing prior to commercialization.”21
Second, hundreds of millions of people have consumed GMOs for over twenty years with no evidence of ill effects and no lawsuits against the GMO manufacturers, even in the United States, which is a litigious nation. If GMOs are a health threat, surely we would have heard by now. Many lawsuits have been filed for the herbicide Roundup but not specifically for the health effects of transgenic crops.22
Third, it has been claimed that the scientific evidence is overwhelmingly in favor of the safety of GMOs in human consumption. In one widely cited review of 1,700 studies, the authors23 state that GMOs are established as safe.24 Another review funded by the agricultural biotechnology industry asserts “the improbability of de novo generation of toxic substances in crop plants using genetic engineering practices.”25
Fourth, any hypothetical risks conjured up by GMO skeptics have not borne out, and any GMO crops that have exhibited significant deficiencies during the breeding process have been rejected by breeders before commercialization.26
Fifth, agencies like the European Food and Safety Authority (EFSA) and the U.S. Food and Drug Administration (FDA) have given GMOs currently on the market a positive safety rating. Society depends on these agencies for many other safety determinations, so why should we not respect their decisions on GMOs? Katy L. Johnson, Alan F. Raybould, Malcolm D. Hudson, and Guy M. Poppy state that “GM crops today in Europe are subject to intense scrutiny and European regulations to assess and address the safety of GM crops with regards to human health and the environment are perhaps the most stringent in the world.”27
Regarding the first argument, GMO skeptics believe that testing done by corporate molecular breeders is largely restricted to the phenotypes with the intended or desired traits for the GM crop, such as agricultural performance. Other tests (for example, those done on crop nutritional components, allergenicity, and possible emergent unanticipated properties) are not fully transparent, often are labeled as confidential business information, and do not report negative findings. Independent toxicologists have found it difficult to obtain isogenic varieties (pure lines with and without the transgene) from seed manufacturers to undertake their own studies.
As for as how rigorous the studies are, at least in the United States, there are no required testing requirements under the 1992 FDA policy. The agency undertakes a “consultation” with a molecular breeder. The FDA classified the new GMOs as generally regarded as safe (GRAS)—a status that is assigned to certain chemical food additives. In its 1992 policy, the FDA wrote: “The agency is not aware of any information showing that foods derived of the new methods [gene splicing] differ from any other foods in any meaningful or uniform way, or that as a class, foods developed by the new techniques present any different or greater safety concern than foods developed by traditional plant breeding.”28
Critics of this policy note that in 1992 little was known about testing GMOs for toxicity. The first products were not commercialized until 1996. So how could FDA know four years before the first products were commercialized that the foreign genetic materials introduced into plants, at random locations in the chromosomes, were GRAS? Moreover, long-term tests of GMOs on animals were not begun until over a decade after the policy was introduced.
The second argument used as evidence of the safety of GMOs for human consumption is that countless people have consumed GMOs for over twenty years with no evidence that any person has been harmed. This is certainly true. There have been no public health advisory warnings, no clinical studies documenting human health effects, and no anecdotal cases of acute toxicity from GMO crops related to the transgenes.
GMO skeptics acknowledge the lack of evidence for acute toxicity in humans. They question the safety of GMOs for chronic toxicity, where testing has been minimal. Fagan, Antoniou, and Robinson write: “Short-term studies are useful for ruling out acute toxicity, but do not provide valid evidence regarding the long-term safety of GMOs. Effects that take a long time to show up, such as cancer, severe organ damage, compromised reproductive capacity, teratogenicity, and premature death, can be reliably detected only in long-term and multigenerational studies.”29
The GMO skeptics also question whether the assessments that are carried out by the seed manufacturers examine the subtle changes in proteins, including nutrients. Consumers might be getting a generally safe food crop with diminished nutritional value, which in the long run could affect human health.
There is a point to be made here. “Junk food,” which is characterized as food that is low in nutritional value and high in calorie content, generally does not exhibit acute effects on consumers but over the long run can be detrimental to their health. The GMO skeptics offer a cornucopia of hypotheticals, including the impact of some GMO proteins (such as the Bt toxins) that show up intact in the human gut. Can they affect the human microbiome adversely? Critics call for assessments of GMOs that investigate the nutritional comparability of the GMO crop with its parental strain. Is there any scientific basis for concern? Although there are not many studies, at least one solid example gives the hypothetical risks some credence. In 1995, Tomoko Inose and Kousaku Murata of the department of applied microbiology at the Research Institute for Food Sciences at Kyoto University showed how a GM yeast exhibited increased toxicity: “The cellular level of methylglyoxal (MG), a highly toxic 2-oxoaldehyde, in Saccharomyces cerevisiae cells transformed with genes … was compared with that in non-transformed control cells.… When these transformed cells were used for alcohol fermentation from glucose, they accumulated MG in cells at a level sufficient to induce mutagenicity. These results illustrate that careful thought should be given to the potential metabolic products and their safety when a genetically engineered yeast is applied to food-related fermentation processes.”30
Regarding the GMO proponents’ point 5—that the scientific studies are overwhelmingly in favor of the safety of GMOs—they are correct. There are more studies that support the null hypothesis—no adverse effects.
GMO skeptics argue that a significant number of the no-effect studies were supported by industry and were based on acute toxicity studies. They were not testing worst-case scenarios and accept as an assumption “substantial equivalence.” When industrial sources analyze the data of studies that report adverse effects of GMOs, they claim that the experiments possess insufficient power (that is, too few animals) to show an effect.
The twentieth-century philosopher Karl Popper noted that falsifying a hypothesis (by using deduction) can yield a definitive result but that confirming a hypothesis (by using induction) cannot. Thus, trying to prove a food is safe is always indeterminate if a case is built by accumulating supporting evidence. If the hypothesis is “The food is safe,” it can be falsified by one piece of reliable evidence—that is, the food caused allergenic reactions in consumers. Even so, the food might be safe for all people who do not have allergies to it. If the hypothesis “The food is not safe” is accepted, then tests needs to be done to falsify the hypothesis and demonstrate that it is safe. Finding that it is allergenic for one individual does not mean that it is allergenic for many. And that is where population studies enter.
How does this translate into toxicology studies? The best evidence that a food is safe is testing the most probable case where it might not be. If it is believed the GMO food is unsafe because it contains the upregulation of a toxicant, then the most sensitive test for the toxin’s effect should be chosen. If the test results are negative, then this is the best evidence to falsify the hypothesis “The food has a dangerous amount of a toxin.” If, however, a test is underpowered or has a low probability of yielding a positive result, then it produces a weak evidentiary claim that there is no risk.
If the starting point is the hypothesis that “GMOs are safe” (that is, substantial equivalence), then what tests would most likely reveal any hazards? Applying the Popperian method of falsification requires making an effort to falsify the hypothesis. Only if it survives the test can it be assumed to be safe. The GMO skeptics argue that this method is not the one currently being used in the United States.
The fourth point made in favor of GMO safety is that plant breeders have considerable experience in eliminating unsafe cultivars before they are introduced into the marketplace. GMO skeptics argue that molecular breeding introduces new possibilities that cannot be observed by plant breeders because the effects might be hidden or subtle, such as changes in a plant’s nutritional properties. Moreover, they ask whether society should place its trust in the manufacturers of a product as a definitive source of its safety. That, they say, would be a conflict of interest, like giving General Motors the final word on the safety of its cars.
Some GMO skeptics outline the tests that would provide public confidence in the transgenic crops: “A full range of ‘omics’ molecular profiling analysis should be carried out … using high-throughput methods, such as microarray analysis, proteomics (study of all proteins produced), and metabolomics (the small molecule metabolites in biological systems) … these ‘omics’ profiling tests must be done on the GMOs, and the isogenic non-GMOs grown at the same location and time, in order to highlight the presence of potential toxins, allergens, and compositional/nutritional disturbances caused by the GM transformation.”31 This view has been supported by the 2016 report of the National Academies of Sciences, Engineering, and Medicine (NASEM) and is discussed in chapter 11.
The FDA has acknowledged some of the possible outcomes of transgenic plants:
Additionally, plants, like other organisms, have metabolic pathways that no longer function because of mutations that occurred during evolution. Products or intermediates of some of these pathways may include toxicants. In rare cases, such silent pathways may be activated by the introduction or rearrangement of regulatory elements, or the inactivation of repressor genes by point mutations, insertional mutations, or chromosomal rearrangements. Similarly, toxicants ordinarily produced at low concentrations in a plant may be produced at higher levels in a new variety as a result of such occurrences. However, the likelihood of such events occurring in food plants with a long history of safe use is low. The potential of plant breeding to activate or upregulate pathways synthesizing toxicants has been effectively managed by sound agricultural practices, as evidenced by the fact that varieties with unacceptably high levels of toxicants have rarely been marketed.32
The operative phrase is “the likelihood of such events occurring in [GMO] food plants with a long history of safe use is low.” Why is this so?
Both GMO critics and noncritics agree that untoward effects can occur with genetically engineered crops. However, noncritics consider that they are unlikely to occur and that if they do occur, they will be eliminated by the breeder. GMO skeptics do not accept the low-probability and low-impact event and thus call for extensive premarket testing: “What are needed are long-term and multigenerational studies on GMOs to see if the changes found in short- and medium-term studies, which are suggestive of harmful health effects, develop into serious diseases, premature death, or reproductive or developmental effects.”33
The final argument for GMO safety is that major agencies of Europe and the United States have approved the safety of GMOs. It is certainly correct that the FDA and the EFSA have unequivocally approved GMOs as safe for human consumption. Some scientific observers, like Johnson, Raybould, Hudson, and Poppy, have stated that “GM crops today in Europe are subject to intense scrutiny and European regulations to assess and address the safety of GM crops with regard to human health and the environment are perhaps the most stringent in the world.”34
GMO skeptics question the independence of these agencies. When some EPA staff scientists opposed approval of GMOs as GRAS without required testing with regard to human health and environmental impacts, they were overruled. Also, EFSA has been heavily criticized, say critics, for the conflicts of interest of its personnel and therefore is not a neutral agency separated from political pressures.
This chapter has reviewed opposing arguments within the scientific community on the human health effects of GMOs. There is general consensus that no GMO product has had an acute effect on consumers but disagreement on whether chronic effects and nutritional changes in genetically engineered foods are possible in current or future products and on whether whole-food animal studies can reveal adverse human health effects. And there is some consensus among different stakeholder groups on the value or feasibility of omics analyses of GE crops for reducing the uncertainty of unanticipated effects.
Notes
1. Andrew Cockburn, “Assuring the Safety of Genetically Modified (GM) Foods: The Importance of a Holistic, Integrative Approach,” Journal of Biotechnology 98 (2002): 83.
2. Andrew Pollack, “U.S.D.A. Approves Modified Potato. Next Up: French Fry Fans,” New York Times, November 7, 2014.
3. John Fagan, Michael Antoniou, and Claire Robinson, GMO Myths and Truths, 2nd ed. (London: Earth Open Source, 2014), http://
4. Council of the European Communities, Council Directive of April 23, 1990 on the Deliberate Release into the Environment of Genetically Modified Organisms, 90/220/EEC.
5. Cockburn, “Assuring the Safety of Genetically Modified (GM) Foods,” 85.
6. Jonathan R. Latham, Allison K. Wilson, and Ricarda A. Steinbrecher, “The Mutational Consequences of Plant Transformation,” Journal of Biomedicine and Biotechnology (2006): 1–7.
7. Nina Federoff and Nancy Marie Brown, Mendel in the Kitchen: A Scientist’s View of Genetically Modified Foods (Washington, DC: Joseph Henry Press, 2004), 174.
8. Latham, Wilson, and Steinbrecher, “The Mutational Consequences of Plant Transformation,” 4.
9. Harry A. Kuiper, Gijs A. Kleter, P. Hub, J. M. Noteborn, and Esther J. Ko, “Assessment of the Food Safety Issues Related to Genetically Modified Foods,” Plant Journal 27, no. 6 (2001): 503–528.
10. Federoff and Brown, Mendel in the Kitchen, 175.
11. Cockburn, “Assuring the Safety of Genetically Modified (GM) Foods,” 93.
12. Organisation for Economic Co-operation and Development, Agricultural Policies in OECD Countries: Monitoring and Evaluation 2000 (Cedex, France: OECD, June 2000), https://www.oecd-ilibrary.org/docserver/agr_oecd-2000-en.pdf?expires=1525810555&id=id&accname=oid006278&checksum=5BA0545A667750F8E2A945394B8E7A7B.
13. Erik Millstone, Eric Brunner, and Sue Mayer, “Beyond ‘Substantial Equivalence,’” Nature 401 (1999): 525–526.
14. Cockburn, “Assuring the Safety of Genetically Modified (GM) Foods,” 94.
15. Fagan, Antoniou, and Robins, GMO Myths and Truths, sec. 2.1, 62.
16. Paul Lurquin, High Tech Harvest: Understanding Genetically Modified Food Plants (Boulder, CO: Westview Press, 2002), 99.
17. Athenix Corporation, “Early Food Safety Evaluation for EPSPS ACES Protein,” submission to the Office of Food Additive Safety, Division of Biotechnology and GRAS Notice Review, HFS-255, Center for Food Safety and Applied Nutrition, Food and Drug Administration, October 7, 2009, http://
18. Lurquin, High Tech Harvest, 102.
19. Cockburn, “Assuring the Safety of Genetically Modified (GM) Foods,” 89.
20. Qixing Mao, Fabiana Manservisi, Simona Panzacchi, Daniele Mandrioli, Ilaria Menghetti, Andrea Vornoli, Luciana Bua, et al. “The Ramazzini Institute 13-Week Pilot Study on Glyphosate Administered at Human-Equivalent Dose to Sprague-Dawley Rats: Effects on the Microbiome,” Environmental Health 17, no. 1 (May 2018), https://
21. Suzie Key, Julian K.-C. Ma, and Pascal M. W. Drake, “Genetically Modified Plants and Human Health,” Journal of the Royal Society of Medicine 101, no. 6 (2008): 292.
22. Carey Gillem, “New Claims against Monsanto in Consumer Lawsuit over Roundup Herbicide,” Huffington Post, June 20, 2017.
23. Alessandro Nicolia, Alberto Manzo, Fabio Veronesi, and Daniele Rosellini, “An Overview of the Last Ten Years of Genetically Engineered Crop Safety Research,” Critical Review of Biotechnology 34, no. 1 (2014): 77–88.
24. Alexander Y. Panchin and Alexander I. Tuzhikov, “Published GMO Studies Find No Evidence of Harm When Corrected for Multiple Comparisons,” Critical Reviews in Biotechnology 37, no. 2 (2017): 213–217.
25. Andrew Bartholomaeus, Wayne Parrott, Genevieve Bondy, and Kate Walker, “The Use of Whole Food Animal Studies in the Safety Assessment of Genetically Modified Crops: Limitations and Recommendations,” Critical Reviews in Toxicology 43, no. 52 (2013): 1–24.
26. Federoff and Brown, Mendel in the Kitchen.
27. Katy L. Johnson, Alan F. Raybould, Malcolm D. Hudson, and Guy M. Poppy, “How Does Scientific Risk Assessment of GM Crops Fit within the Wider Risk Analysis,” Trends in Plant Science 12, no. 1 (2006): 1–5.
28. U.S. Food and Drug Administration, “Statement of Policy: Foods Derived from New Plant Varieties,” Federal Register 57, no. 104 (1992): 22,991.
29. Fagan, Antoniou, and Robinson, GMO Myths and Truths, sec. 2.2.
30. Tomoko Inose and Kousaku Murata, “Enhanced Accumulation of Toxic Compound in Yeast Cells Having High Glycolytic Activity: A Case Study on the Safety of Genetically Engineered Yeast,” International Journal of Food Science and Technology 30 (1995): 141–146.
31. Fagan, Antoniou, and Robinson, GMO Myths and Truths, sec. 2.2.
32. David A. Kessler, Michael R. Taylor, James H. Maryanski, Eric L. Flamm, and Linda S. Kahl, “The Safety of Foods Developed by Biotechnology,” Science 256 (1992): 1832.
33. Fagan, Antoniou, and Robinson, GMO Myths and Truths, sec. 2.2.
34. Johnson, Raybould, Hudson, and Poppy, “How Does Scientific Risk Assessment of GM Crops Fit within the Wider Risk Analysis,” Trends in Plant Science 12, no. 1 (2006): 1–5.