Consumer Policy Institute/Consumers Union
Food is fundamentally different from other consumer products. As something we literally take inside ourselves, that is necessary on a daily basis for growth and life, and that is bound up in our cultures and traditions, we care about it intensely. Consumers feel they have a fundamental right to know what they are eating, and that it is safe. Most developed countries have adopted laws that reflect this view, requiring ingredient labeling, labeling as to any processing (e.g., frozen, homogenized, irradiated), conformance to standards of identity (e.g. peanut butter must be made from peanuts), and indicating presence of any additives (e.g. sulfites, preservatives). Some countries require labeling as to the fat, protein, carbohydrate and vitamin content of food as well.
All of this labeling serves the consumer's right to know, and is above and beyond underlying national programs to assure the safety of food from such things as hazardous pesticides residues and additives, and disease-causing bacteria.
Consumers want to know what they are eating both as a pure matter of taste and preference, and for many health-related reasons. They may want to eat fish to improve their chances of avoiding heart disease, or avoid fish because they are concerned about depletion of certain species in the oceans or about mercury contamination. Body builders may seek out red meat, vegetarians will avoid it, and Muslims will avoid pork but not lamb. Mothers may look for apple juice for their children because it is a natural drink, or avoid it because it gives their child a stomachache. Every day, millions of consumers worldwide read millions of food labels and make millions of decisions like this for themselves and their families.
Consumers also have a right to know if food is genetically engineered, both as a matter of taste and preference, and for important health related reasons.
The countries of the European Union have recognized this, and have instituted regulations requiring labeling of all genetically engineered food, although many consumer and environmental groups think the labeling requirements do not go far enough. In the United States, where genetically engineered corn, soybeans and potatoes are being grown commercially, repeated public opinion surveys show consumers overwhelmingly want labeling, but thus far the government has failed to require it. Most countries have not considered the issue yet. Of the large chemical/biotechnology companies that are developing these foods, some, like Novartis, support labeling, but most, like Monsanto and other major developers, oppose it.
The Codex Alimentarius, an agency of the United Nations World Health Organization and Food and Agriculture Organization, is considering whether to adopt a guideline recommending that all countries require labeling of genetically engineered food. Codex guidelines are not binding, but are often adopted by developing countries and can be used to settle trade disputes (if a country adopts a Codex standard, that standard cannot be challenged as protectionist).
Consumers want, and have a right to labeling of all genetically engineered food, because it is not "substantially equivalent" to conventional food, because some individuals can have unpredictable mild to severe allergic reactions, because it can have unanticipated toxic effects, because it can change the nutrition in food, because it can cause dramatic environmental effects and because consumers presently use food labeling to express a wide variety of religious, ethical and environmental preferences.
Genetically Engineered Food is Different
A strawberry that contains a flounder gene that makes it frost resistant, and a bacterial gene that confers antibiotic resistance, and a virus gene that "turns on" the other added genes, is, in the opinion of consumers, fundamentally different from a conventional strawberry. Under normal circumstances, a strawberry can only acquire genetic material from other strawberries--that is, plants of the same species. With genetic engineering, however, scientists can give strawberries genetic material from trees, bacteria, fish, pigs, even humans if they chose to. Where the donor organism and recipient organism are from different species, the resulting genetically engineered organism is called "transgenic."
Some people-mostly scientists and corporations involved in the development of genetically engineered food-argue that the strawberry with the foreign genes is not really different. In the language of the Codex and international regulation, it is "substantially equivalent" and therefore needs no label. Consumers, however, (1) through their organizations, (2) through comments to regulators, and (3) through opinion surveys, have repeatedly expressed the view that this strawberry, and all other genetically engineered foods, are not "substantially equivalent," but are sufficiently different that (like irradiated foods, and foods containing additives), they should be labeled. Since labeling laws are created to meet consumer needs, it is consumer opinion, which should be relevant in this regard.
A range of consumer and other civil society organizations worldwide argue that any plant or animal food to which genes have been added from a source other than the species to which the food belongs, should be required to be labeled as genetically engineered. This is because it is different from conventional food; in the language of Codex, it is not "substantially equivalent" to unengineered food.
Genetically Engineered Food Can Cause Toxic Effects
The fact that genetic engineering can go seriously wrong was shown by one of the very first products introduced into the market. An amino acid called tryptophan was sold in a number of countries including the United States as a dietary supplement. In the late 1980s, the Showa Denko company of Japan began making tryptophan by a new process, using genetically engineered bacteria, and selling it in the United States. Within a period of months, thousands of people who had taken the supplement began to suffer from eosinophilia myalgia syndrome, which included neurological problems. Eventually at least 1500 people were permanently disabled and 37 died (Mayeno and Gleich, 1994).
As doctors encountered this syndrome, they gradually noticed that it seemed linked to patients taking tryptophan produced by Showa Denko. However, it took months before it was taken off the market. Had it been labeled as genetically engineered, it might have accelerated the identification of the source of the problem.
Showa Denko refused to cooperate in any U.S. government efforts to investigate the cause of the problem. However, the Showa Denko tryptophan that caused the problem was determined to contain a toxic contaminant which appears to have been a byproduct of the increased tryptophan production of the genetically engineered bacteria (Mayeno and Gleich, 1994).
There are many ways besides this in which genetic engineering could go awry and result in hazardous toxins in food. Many common plant foods such as tomatoes and potatoes produce highly toxic chemicals in their leaves, for example. Any responsible company working with such plants would check for any changes in toxin levels. But not all companies are equally responsible, and as the Showa Denko example shows, and a serious hazard can be missed.
Government agencies also cannot be counted on to prevent unexpected problems. Worldwide, government premarket safety reviews of genetically engineered products currently ranges from relatively thorough in the European Union, to no review at all in much of the world. In the United States, the government only conducts premarket safety reviews if requested to by the company.
We can expect that in the future genetically engineered food will be developed and grown in many countries, many of them with no premarket safety reviews. Consumers want labeling of genetically engineered food because unless all such products are labeled, it will be extremely difficult to determine the source of any toxin problems originating in such food.
Genetically Engineered Food Can Cause Allergic Reactions
In the United States, about a quarter of all people say they have an adverse reaction to some food (Sloan and Powers, 1986). Studies have shown that 2 percent of adults and 8 percent of children have true food allergies, mediated by immunoglobin E (IgE) (Bock, 1987; Sampson et al., 1992). People with IgE mediated allergies have an immediate reaction to certain proteins that ranges from itching to potentially fatal anaphylactic shock. The most common allergies are to peanuts, other nuts and shellfish.
Allergens can be transferred from foods to which people know they are allergic, to food that they think is safe, via genetic engineering. In March 1996, researchers at the University of Nebraska in the United States confirmed that an allergen from Brazil nuts had been transferred into soybeans. The Pioneer Hi-Bred International seed company had put a Brazil nut gene that codes for a seed protein into soybeans to improve their protein content for animal feed. In an in-vitro and a skin prick test, the engineered soybeans reacted with the IgE of individuals with a Brazil nut allergy in a way that indicated that the individuals would have had an adverse, potentially fatal reaction to the soybeans (Nordlee et al., 1996).
This case had a happy ending. As Marion Nestle, the head of the Nutrition Department at New York University summarized in an editorial in the respected New England Journal of Medicine, "In the special case of transgenic soybeans, the donor species was known to be allergenic, serum samples from persons allergic to the donor species were available for testing and the product was withdrawn" (Nestle, 1996: 726). However, for virtually every food, allergists will tell you, there is someone allergic to it. Proteins are what cause allergic reactions, and virtually every gene transfer in crops results in some protein production. Genetic engineering will bring proteins into food crops not just from known sources of common allergens, like peanuts, shellfish and dairy, but from plants of all kinds, bacteria and viruses, whose potential allergenicity is largely uncommon or unknown. Furthermore, there are no foolproof ways to determine whether a given protein will be an allergen, short of tests involving serum from individuals allergic to the given protein. This point is strongly driven home in the case of the transgenic soybean containing a Brazil nut gene referred to above: where animal tests had suggested that the transferred Brazil nut seed storage protein was not an allergen (Nordlee et al., 1996). Had the results of the animal tests been relied on and the soybeans approved, the results could have been disastrous.
However, most biotechnology companies increasingly use microorganisms rather then food plants as gene donors or are designing proteins themselves, even though the allergenic potential of these proteins is unpredictable and untestable. Consequently, Nestle continues, "The next case could be less ideal, and the public less fortunate. It is in everyone's best interest to develop regulatory policies for transgenic foods that include premarketing notification and labeling" (Nestle, 1996: 727).
To adequately protect consumer health from the effects of unrecognized or uncommon allergens, all genetically engineered food must be labeled. Otherwise there will be no way for sensitive individuals to distinguish foods that cause them problems from ones that do not. This need is particularly urgent, since one of the potential consequences is sudden death, and the most affected population is children.
Genetic Engineering Can Increase Antibiotic Resistance
Genetic engineering, despite the precise sound of its name, is actually a very messy process, and most attempts end in failure. While the gene to be transferred can be identified fairly precisely, the process of inserting it in the new host is often very imprecise. Genes are often moved with something that is the molecular equivalent of a shotgun. Scientists coat tiny particles with genetic material and then "shoot" these genes into thousands of cells in a petri dish before they get one where the desired trait "takes" and is expressed. Because the transferred trait, such as ability to produce an insecticide in the leaves of the plant, is often not immediately apparent, scientists generally also must insert a "marker gene" along with the desired gene into the new plant. The most commonly used marker gene is a bacterial gene for antibiotic resistance. Most genetically engineered plant food contains such a gene.
Widespread use of antibiotic resistance marker genes could contribute to the problem of antibiotic resistance. Antibiotic resistance genes may move from a crop into bacteria in the environment. Since bacteria readily exchange antibiotic resistance genes, such genes could eventually move into disease-causing bacteria and make them resistant to a given antibiotic and therefore harder to control. It is already known that bacteria can take up naked DNA in a suitable environment, so antibiotic resistance genes could theoretically be transferred in the digestive tract to bacteria. A genetically engineered Bt maize plant from Novartis includes an ampicillin-resistance gene. Ampicillin is a valuable antibiotic used to treat a variety of infections in people and animals. A number of European countries, including Britain, have refused to permit the Novartis Bt corn to be grown, over health concern that the ampicillin resistance gene could move from the corn into bacteria in the food chain, making ampicillin a far less effective weapon against bacterial infections. The fact that the ampicillin resistance gene is connected to a bacterial promoter (a genetic "on" switch) rather than a plant promoter in the Novartis Bt corn could improve the chances that it if the gene moved into bacteria it could be readily expressed. In September 1998, the British Royal Society put out a report on genetic engineering that called for the ending the use of antibiotic resistance marker genes in engineered food products (Anonymous, 1998).
Some consumers may wish to avoid plants with antibiotic resistance marker genes.
Genetically Engineered Food Can Create Environmental Risk
To a great extent, the size of the potential environmental risk associated with the growing of genetically engineered crops is roughly proportional the total area cultivated. In addition, there are ecological risks associated with large-scale release that will not be detected by small-scale studies. Thus, to fully understand these risks requires knowledge of the acreage of genetically engineered crops. Tables 1-3 show the global area of transgenic crops in 1996 and 1997, by country, by trait and by crop/engineered trait. The tables show that significant areas of transgenic crops are grown in both the industrialized and developing countries and that the area devoted to transgenic crops is increasing rapidly. Between 1996 and 1997, the total global area increased more than 4.5-fold, from 2.8 to 12.8 million hectares.
Transgenic crops are not grown just in the developed countries. Table 1 shows that two developing countries, Argentina and China, contained 43 percent of the global area in 1996; the figure declines to 25 percent in 1997.
Furthermore, as can be seen in Table 4, field trials involving transgenic crops have occurred in some 45 countries in all regions of the world, including Africa, Asia, and Latin America. This shows the potential ecological problems associated with cultivation of transgenic crops are not solely restricted to the developed countries and is something that many developing countries will have to deal with.
Just three traits-herbicide tolerance, insect resistance, and virus resistance-account for virtually all the global area in transgenic crops (Table 2). The relative area planted with the three traits has changed drastically, however. In 1996, virus resistance was the most widespread trait, occurring in 40 percent of global area in transgenic crops in 1996, followed closely by insect resistance, at 37 percent, and herbicide tolerance at 23 percent. In 1997, herbicide tolerance was the most widespread, occurring in 54 percent of the global area, followed by insect resistance and virus tolerance. The big change between 1996 and 1997 was the more than ten-fold expansion (from 600,000 hectares to 6.9 million hectares) in area of herbicide tolerant crops, primarily due to Monsanto's RoundUp Ready soybeans in the U.S. and herbicide tolerant canola (or oilseed rape) in Canada. The dominance of virus tolerance in 1996 was virtually all due to the extensive area in transgenic virus-tolerant tobacco in China.
Each crop trait poses certain unique environmental hazards. In addition, all three traits pose a common hazard: movement of the engineered trait or gene into the same crop type or to its wild relatives. We'll deal with the unique environmental hazards first, followed by a discussion of the common hazard.
Herbicide-tolerant (HT) crops are varieties on which herbicides can be used to kill weeds, without killing the crop itself, such as corn, soybeans, cotton, or oilseed rape (canola). These varieties encourage pesticide dependency by requiring farmers to use herbicides, which frequently pollute groundwater and can cause various forms of ecological damage. In the developed countries, where the herbicide market for most crops is saturated, HT crops encourage farmers to switch from one herbicide to another, while in the developing countries, where the market for herbicides is rapidly growing, HT will lead to increased herbicide use. In either case, no attention is paid to other more sustainable means of weed control that do not rely on synthetic herbicides, such as intercropping, mulching, use of green manures, etc.
The fact that HT crops represent over half of the global area sown to transgenic crops is not surprising given the fact that the transnational corporations--such as Monsanto, Novartis and DuPont--that have developed these crops are major herbicide producers. These same companies have also bought up numerous seed companies and so are producing transgenic seeds that are dependent on the parent company's herbicides. Monsanto, for example produces two of the top selling herbicides in the world: glyphosate and alachlor. In the first half 1998, Monsanto, spent some $6 billion dollars buying two the world's top 10 seed companies, DeKalb Plant Genetics and Cargill's international seed business; the world's largest cotton seed company Delta & Pine Land; and Plant Breeding International (RAFI, 1998). With these purchase Monsanto became the world's second largest seed company. In June, 1998, Monsanto merged with American Home Products and bypassed Novartis to become the world's largest agrochemical firm. Novartis is also the third largest seed company. Given this high level of monopolization of the seed industry by the world's largest agrochemical companies, we can expect the focus on HT crops to continue to dominate the global acreage of transgenic crops.
Insect-resistant crops have been engineered to produce substances that kill or repel insect pests. Virtually all such crops contain a modified gene from the soil bacterium Bacillus thuringiensis (Bt) which causes the plant to produce an active form of an endotoxin throughout the plant, including leaves and fruit. The bacterium itself has long been used, especially by organic farmers, as a relatively harmless natural insecticide. It is also widely used in the United States and Europe by more conventional farmers who use integrated pest management to minimize use of more toxic chemicals. Indeed, Bt sprays are used on over 2 million acres of crops in the U.S. (Union of Concerned Scientists, 1998). Now, however, transgenic Bt corn, cotton, potatoes, tomatoes and rice are all being grown in various parts of the world, although Bt cotton is the most widespread (James, 1997).
While Bt crops at first glance appear to be ecologically sound, because they reduce the need, at least in the short term, for chemical pesticides, they have serious drawbacks. Crops that continuously produce Bt endotoxin quickly speed up the process of the spread of genetic resistance to the Bt endotoxin among the pests feeding on the crops. Scientists predict that Bt could become relatively useless, however, within a few years of widespread planting of Bt crops (Gould, 1988, 1991). If resistance to Bt becomes widespread in the U.S., then organic farmers would have few alternative pesticides to control pests formerly controlled by Bt, while conventional farmers would have to turn to more toxic pesticides, thereby potentially leading to increased levels of pesticide residues. A recent computer model of Bt corn developed by a scientist at the University of Illinois in the U.S. predicted that if all U.S. farmers grew Bt corn, resistance would develop in only a single year (Burghart, 1998)! Scientists at the University of North Carolina in the U.S. have found Bt resistance genes in wild populations of a moth pest that feeds on corn (Gould et al. 1997).
In the U.S. concern over the evolution of resistance to Bt was strong enough that the EPA required functioning resistance management plans as a condition for permitting the commercial sale of Bt cotton in 1996. The companies were also asked to develop resistance management plans for other Bt crops such as Bt corn and Bt potatoes. In the first two years of planting, the Bt cotton crop in both the US and Australia had many problems (Benbrook and Hansen, 1997). The resistance management plan had clearly failed in the case of US cotton. In 1997, a coalition of groups, including the International Federation of Organic Agriculture Movements, Greenpeace International, and the Center for Technology Assessment petitioned the U.S. EPA to take the transgenic Bt crops off the market because of the threat they pose to organic farmers and the environment. If the EPA does not take action on this petition by September 30, 1998, the groups have threatened to sue.
There is also concern that the difference in the endotoxin as produced in a transgenic plant compared to what occurs naturally in the bacterium may cause ecological disruption due to toxicity to beneficial insects and other non-target organisms. In the natural form, the bacteria contain the endotoxin in the form of a long crystallized protein, which is partially digested in the insect's stomach to release an activated form of the endotoxin. This activated endotoxin punches holes in the insect's digestive tract. It is the activated, or truncated, form of the endotoxin that has been engineered into plants. Since this activated form only occurs in the guts of certain insects, few other organisms have been exposed to it. Thus its effect on these non-target organisms is unknown and may be negative.
Researchers from the Swiss Federal Research Station for Agroecology and Agriculture found over a two-thirds increase in mortality of green lacewing larvae (a major predator of maize pests) fed either European corn borer or armyworm larvae raised on Novartis' Bt maize, compared to lacewing larvae fed moth larva raised on non-transgenic maize (Hillbeck et al., 1998). Furthermore, the increased lacewing mortality was seen regardless of whether it ate sick prey (i.e. poisoned by eaten Bt) or healthy (i.e. resistant to Bt) prey. Bt-resistant insects could feed on Bt maize, fly off to other plants, and be eaten by a lacewing which would then die, resulting in ecological effects that extend beyond the borders of the area planted to transgenic crops.
In Thailand, where trials of Monsanto's Bt cotton began in 1996, the committee in charge of the field trials was told that 40 per cent of the bees died during a contained trial (Compeerapap, 1997). Since no further information has been released, it is not known if the bee mortality was a result of the Bt cotton or not.
According to data submitted to the US Environmental Protection Agency, Novartis' Bt corn also harmed springtails (Collembola), which are flightless insects that feed on fungi and debris in soil and, as decomposers, are considered to be a beneficial insect (EPA MRID No. 434635). Other studies have shown that the Bt toxin can persist in soils for over forty days (the longest time evaluated) and can retain its toxicity to insects (Koskella and Stotzky, 1997). Thus, continuous production of Bt endotoxin in Bt crops could lead to a soil build up of Bt that could both enhance development of resistance to Bt as well as have toxic effects on non-target organisms.
Bt crops are not the only insect resistant plants have been shown to have toxic effects on beneficial insects. Experiments done in Scotland with transgenic potatoes that contained a gene for the snow drop lectin (lectins are a class of proteins known to resist insect digestion) showed that ladybird beetles that ate aphids reared on the transgenic potatoes laid 38 percent fewer eggs and lived half as long as ladybirds fed aphids reared on non-transgenic potatoes (Birch et al., 1997). Furthermore, male ladybirds fed aphids reared on transgenic potatoes had lower fertility compared to a male fed aphids reared on non-transgenic potatoes.
Virus-resistant crops almost all contain genes from a virus that confer resistance to that same virus. However, these genes can mix with genes from other viruses that naturally infect the plant to create new gene combinations, some of which can give rise to new or deadlier viruses. US and Canadian work has shown that wild viruses can hijack genes from engineered crops at rates far higher than previously suspected. In one experiment, researchers from Agriculture Canada infected a plant with a "crippled" cucumber mosaic virus that lacked the gene that allowed the virus to move between plant cells. They then took the equivalent "movement" gene from another virus and put it into the same plants. Less than two weeks later, the scientists found functioning mosaic viruses in one of eight plants, thereby demonstrating that gene mixing between viruses can occur (Kleiner, 1997). The concern was great enough that the U.S. Department of Agriculture held a meeting in October, 1997 to discuss possible restrictions aimed at reducing the risk of creating harmful new plant viruses due to the use of virus-resistant crops (Kleiner, 1997).
A common serious concern with all the transgenic crops is that the genes for the engineered traits (or transgenes) will move into other plants--either of the same type or into closely related species. When transgenes move into plants of the same type, this is considered as "gene pollution" or "genetic smog." Organic and conventional farmers in Europe and America are concerned about this because genetically engineered organisms are not considered as organic foods, and in Europe where there is a growing market for nontransgenic foods, so that flow of transgenes into their crops could render them not saleable as organic or nontransgenic. Experiments in Germany with engineered oilseed rape have shown that its pollen moved some 200 meters into nonengineered oilseed rape plants (Ostermann, 1997). Four German farmers have taken the Robert Koch Institute in Berlin to court to demand that they stop field trials of transgenic oilseed rape to prevent flow of transgenes into their crops.
"Gene pollution" is especially problematic for the Southern countries where the center of origin for many crops are. In these areas, traditional crop varieties could become "polluted" with genes from the genetically engineered crops. In Thailand, the government decided to cancel field tests of Monsanto's Bt cotton in part in response to concerns raised that transgenes could flow from this cotton into some of the 16 plants in the cotton family identified by the Institute of Traditional Thai Medicine that traditional healers use as medicines and that no research was being done to address to test this concern (Anonymous, 1997).
Further, the rate of gene flow between crop plants and their wild relatives may be higher than normally thought. Researchers in the southern United States demonstrated that more than 50% of the wild strawberries growing within 50 meters of a strawberry field contained marker genes from the cultivated strawberries. Researchers in central U.S. found that after ten years more than a quarter of the wild sunflowers growing near fields of cultivated sunflowers had a marker gene from the cultivated sunflowers; after 35 year old system, the figure was 38 percent (Kling, 1996).
If genes flow into populations of wild relatives that enhance their fitness, superweeds could be created. In fact, some 11 of 18 of the most serious weed species worldwide are also grown as crops (Holmes et al., 1977). If the gene for herbicide tolerance escapes into wild relatives of crop plants that are weeds, it could result in a new generation of herbicide-tolerant superweeds. If the gene for the production of the Bt endotoxin moves into wild plants, they could become resistant to butterfly, moth and beetle pests, just like the Bt crops. This could upset established ecological balances by either causing the wild plant to flourish excessively and become a weed, or be reducing the butterfly or moth population that previously fed on the newly toxic plant. If a gene that confers virus resistance to a crop escapes, through pollination into a wild relative, that relative too can become virus resistant and become a super weed.
Data from the past three years with oilseed rape clearly demonstrates that herbicide tolerance transgenes, which have the greatest potential to create superweeds, can easily flow into wild weedy relatives. Work in Denmark with oilseed rape resistant to glufosinate (common tradename BASTA) showed that the resistance appeared in field mustard, a wild weedy relative, grown near transgenic HT oilseed rape in as little as one generation (Mikkelsen et al., 1996). These crop/weed hybrids were fertile. Scientists hypothesized that the crop/weed hybrids would generally be less hardy than pure weeds as crops are weaker plants than weeds. More recent work, carried out in a greenhouse in the United States has demonstrated that even under conditions most favorable to the weed, the glufosinate-tolerant oilseed rape/weed hybrid was resistant to glufosinate and was just as fertile as the weed (Snow and Jorgensen, 1998). This work shows that the genetic cost of the herbicide tolerance gene are negligible and that the transgene could persist in the weed population even in the absence of selection due to herbicide application.
A recent experiment has shown that herbicide tolerance genes may have quite unexpected ecological effects that could dramatically increase the possibility of a "super weed" being created by genetic engineering. Resistance to the herbicide chlorsulphuron was inserted into Arabidopsis thaliana plants, either by genetic engineering or by a form of classical breeding called mutation breeding (Begelson et al., 1998). The engineered plants were roughly 20 times more likely to outcross with other A. thaliana plants than the ordinary mutants. Thus, the act of genetic engineering dramatically increased gene flow, and functionally turned a species that normally only mates with itself into an outcrosser. The authors do not know how to relate there results to transgenic HT crops, but point out that this transgene has been introduced into dozens of agricultural crops and is promoted as a selectable marker for transgenic plants.
Labeling of genetically-engineered food is therefore needed so that consumers who care about these environmental risks can exercise their preference and avoid these foods.
Genetic Engineering Can Affect Dietary Preferences
Consumers make decisions about what they eat for a wide variety of religious, ethical, philosophical and emotional reasons. Most major world religions involve some rules or traditions as to food. Jews and Muslims do not eat pork; Christians often avoid meat on Fridays or during Lent, many Buddhists are strict vegetarians. Many other individuals have food preferences that are not related to an organized religion but which reflect deeply held personal beliefs nevertheless, such as wanting to protect the environment. Groups like Consumers International, Greenpeace International and the International Federation of Organic Agriculture Movements (IFOAM) support labeling of genetically engineered food in order to allow consumers the opportunity to exercise their religious and ethical preferences. For example, the presence of pig genes in lamb (a product not yet on the market, but well within the current capabilities of science) may be of concern to some religious individuals. For those labeling would be essential.
Science is Fallible
When a new technology of food production emerges, it is not always the case that all the problems it may cause are foreseen. To take one recent past example, when pesticides were first synthesized and used widely in the 1950s, they were heralded as a miracle cure for pest problems. Only later did we discover that some of them could also cause birds to lay eggs with shells that collapsed, humans to get cancer, and ultimately insects to become resistant to them.
Genetic engineering is shuffling the deck of genes in ways that are entirely new, and creating living things that have never before existed. Consumers International believes consumers have a right to take a cautious "go slow" approach, and avoid genetically engineered food until more is known about it, if that is what they desire.
Anonymous, 1997. Thailand: Government passes up pest-free cotton plant. IPS.
-------------------1998. Call for UK genetic food watchdog. Nature online service. Sept. 3.
Benbrook, C.M. and M. Hansen, 1997. Return to the "Stone Age of Pest Management." Remarks presented to the EPA Public meeting, "Plant Pesticides Resistance Management," March 21, 1997, Washington, D.C.
Bergelson, J., Purrington, C.B. and G. Wichmann. 1998. Promiscuity in transgenic plants. Nature, 395 (6697): 25.
Birch, A.N.E., Geoghegan, I.E., Majerus, M.E.N., Hackett, C. and J. Allen. 1997. Interactions between plant resistance genes, pest aphid populations and beneficial aphid predators. 1996/7 Scottish Crop Research Institute Annual Report, pp. 66-72. Invergowrie, Dundee, Scotland.
Bock, S.A. 1987. Prospective appraisal of complaints of adverse reactions to foods in children during the first 3 years of life. Pediatrics, 79: 683-688.
Compeerapap, J. 1997. The Thai debate on biotechnology and regulations. Biology and Development Monitor, 32: 13-15.
Gould, 1991. The evolutionary potential of crop pests. American Scientist, 79: 496-507.
Green, A.E. and R.F. Alison. 1994. Recombination between viral RNA and transgenic plant transcripts. Science, 263: 1423-1425.
Hilbeck, A., Baumgartner, M., Fried, P.M. and F. Bigler. 1998. Effects of transgenic Bacillus thuringiensis corn-fed prey on mortality and development time of immature Chysoperla carnea (Neuroptera: Chrysopidae). Environmental Entomology, 27(2): 480-487.
Hileman, B. 1995. Views differ sharply over benefits, risks of agricultural biotechnology. Chemical and Engineering News, August 21, 1995.
Holm, L., Plunknett, D.L., Poncho, J.V. and J.P. Herberger. 1977. The World's Worst Weeds: Distribution and Biology. Honolulu (HI): University Press of Hawaii.
Koskella, J. and G. Stotzky. 1997. Microbial utilization of free and clay-bound insecticidal toxins from Bacillus thuringiensis and their retention of insectidical activity after incubation with microbes. Applied and Environmental Microbiology, 63(9): 3561-3568.
James, C. 1997. Global Status of Transgenic Crops in 1997. ISAAA Briefs No. 5. The International Service for the Acquisition of Agri-biotech Applications (ISAAA): Ithaca, NY. 31 pp.
Jorgensen, R. and B. Andersen. 1995. Spontaneous hybridization between oilseed rape (Brassica napus) and weed Brassica campestris: a risk of growing genetically engineered modified oilseed rape. American Journal of Botany, 81: 1620-1626.
Kling, J. 1996. Could transgenic supercrops one day breed superweeds? Science, 274: 180-181.
Mayeno, A.N. and G.J. Gleich. 1994. Eosinophilia myalgia syndrome and tryptophan production: a cautionary tale. TIBTECH, 12: 346-352.
Mikkelsen, T.R., Andersen, B. and R.B. Jorgensen. 1996. The risk of crop transgene spread. Nature, 380: 31.
Nestle, M. 1996. Allergies to transgenic foods-Questions of policy. The New England Journal of Medicine , 334(11): 726-727.
Nordlee, J.A., Taylor, S.L., Townsend, J.A., Thomas, L.A. and R.K. Bush. 1996. Identification of a brazil-nut allergen in transgenic soybeans. The New England Journal of Medicine , 334(11): 688-692.
Ostermann, D. 1997. GE-rapeseed escapes into environment. Ministry: seeds change normal plants. Frankfurter Rundshau, December 6.
Sampson, H.A., Mendelson, L. and J.P. Rosen. 1992. Fatal and near-fatal anaphylactic reactions to food in children and adolescents. The New England Journal of Medicine , 327: 380-384.
Sloan, A.E. and M.E. Powers. 1986. A perspective on popular perspections of adverse reactions to foods. Journal of Allergy and Clinical Immunology, 78: 127-133.
Snow, A.A. and R.B. Jorgensen. 1998. Costs of transgenic glufosinate resistance introgressed from Brassica napus into weedy Brassica rapa. Paper presented at the Annual meeting of the Ecological Society of America, August.
** NOTICE: In accordance with Title 17 U.S.C. Section 107, this material is distributed for research and educational purposes only. **
Last Updated on 5/24/99
By Karen Lutz