A news item in a recent issue of New Scientist reported a sobering attempt to calculate the true costs of production agriculture in the UK (Pearce, 1999). When currently externalized costs were included in the sum, Jules Pretty and colleagues conservatively estimated that the true cost of UK agriculture - £2.3 billion per year or £208 ha -1 - was roughly equal to the value of the food actually produced by UK agriculture, in other words, a 1:1 ratio of benefits and costs.
An older study by Pimentel et al. (1992) focused on calculating the true benefit:cost ratio of biocide use in US agriculture. When they factored in currently externalized costs, the benefit:cost ratio dropped from a respectable 4:1 based on direct costs only, to 1.3:1(1), just above breakeven. Roughly two thirds of the externalized costs were exacted from society at large - involuntarily.
In the not too distant future, some group of clever scientists will do a full cost accounting of the benefits and costs of GE agriculture. And what will they find? Will we even be able to claim a "break even" outcome? And who will bear the externalized costs - the farmers who grew the GE products or the consuming public who involuntarily supported them through their taxes? Or will those who researched and promoted GE - knowing full well that environmental and food safety risks have not been meaningfully assessed - be held accountable, like the tobacco industry?
I reject the premise that scientists must wait until something goes wrong before acting, particularly when the consequences are potentially severe. Accordingly, let us start from the position that we in the publicly funded scientific community have a responsibility to objectively assess the risks as well as the benefits of agricultural genetic engineering, in an assertive and pro-active fashion, for the benefit of the society that pays us.
Examples of process risks will include:
1) the legacy of ecological, agronomic, and other hazards induced by the narrow disciplinary focus on molecular genetics during the process of industry development;
2) the logistical, agronomic, and other implications of the randomness of transgene insertion and resultant trait instability;
3) unintended secondary gene expression induced by transgene insertion, impacting on agronomic and ecological, and potentially, food safety risks; and
4) horizontal gene transfer, with specific emphasis on the intestines as a portal for gene flow - a concept which is wholly unanticipated in the risk assessment protocols used by Canadian regulators.
Technology should build on science, not the other way around. The science which underlies these issues and which now appears almost weekly in Nature, Science, and PNAS, could and should have appeared in refereed journals before, not after, this technology was commercialized.
The decision to intentionally restrict participation in the process of developing "bio-technology" to primarily molecular geneticists, as documented in Susan Wright's text Molecular Politics, has yielded the legacy of unresolved, and potentially insoluble problems facing ag GE today.
Table 1. Examples of the complications introduced into commercial ag GE by the failure to include real world disciplines in the development of the industry
| Untested and Since Invalidated Assumptions | Missing Disciplines | Relevant Research Challenges |
| of the high dose/refugia model for resistance management in Bt crops (e.g. major resistance genes will be very rare; resistance will be recessive; refuge will supply susceptible mates) | entomology, agronomy, ecology | Tabashnik et al., 1997
Huang et al., 1999 Liu et al., 1999 "None of the essential assumptions of the high dose/refugia strategy have been verified for BT corn" (Andow and Hutchison (1998) |
| that transgenic DNA would rapidly degrade in the gut | physiology, biochemistry, nutrition | Schubbert et al., 1997
Doerfler and Schubbert, 1998 Schubbert et al., 1998 Mackenzie, 1999 |
| that transgenes would affect only the intended target trait, and would not meaningfully affect expression of other genes in the host genome | plant breeding | Bergelson et al., 1998
De Neve et al., 1999 Ho et al., 1999 Kaniewski and Thomas, 1999 |
| that horizontal gene transfer was a non-issue as a vehicle to ramify transgenic traits throughout an ecosystem | microbial ecology, virology, pathology | Hoffmann et al., 1994
Ho, 1998 "if one does not want a gene to be horizontally transmitted....one should better not put "hazardous" genes onto plasmids or transposons" ( Bergmans, 1992) |
| that the possibility of, and implications of, sexual transfer of transgenic traits to wild relatives, here and abroad were non-issues | plant breeding, evolutionary genetics | various, in Traynor and
Westwood, 1999
Desplanque et al., 1999 |
| that hybridisation and transformation events would be rare and hence inconsequential, disregarding the question of probabilities and scale of exposure | landscape ecology, statistics | van Damme, 1992 |
| that unconstrained dispersal of transgenes into both neighboring fields and into nature was inconsequential | plant breeding, entomology, evolutionary genetics, wildlife biology | Losey et al., 1999
Muir and Howard, 1999 |
2. Imprecision and Instability Although "precise" is a characteristic often claimed by genetic engineers, the process of transgene insertion into a new host genome is anything but precise. Indeed, the point at which a transgene inserts itself within a host genome is virtually random, and hence, unrepeatable. It is not yet possible to predict even on which chromosome the transgene(s) will land, let alone where it will insert on a given chromosome. But order matters, not simply to the stability and level of expression of the target trait but also to the expression of other, unrelated traits within the host genome. Thus, unless and until a process is found not just to insert transgenes, but to reliably insert transgenes into predetermined genomic locations, the stability and expression of transgenes will remain problematic.
Even successfully inserted transgenes are commercially worthless without stable and reliable expression. Indeed, it has been argued that the genome of many species is in fact a melange of naturally occurring DNA insertion events, with the key issue not insertion, but expression. It follows, then, that ensuring expression of the desired trait may well be a more demanding problem than transgene insertion itself. In their aptly titled review article "Genome intruder scanning and modulation systems and transgene silencing", Kumpatia et al. (1998) presented evidence of the ability to distinguish self from non-self at the nucleic acid level. They stated that:
"The widespread occurrence of transgene inactivation in plants....suggest that all genomes contain defense systems that are capable of monitoring and manipulating intrusive DNA"
As evidence, they noted that "although a vast number of genetically engineered plants has now been produced, many examples exist in which the introduced gene is not functioning (i.e. is silenced), or is functioning aberrantly."
Unstable expression is of far more than academic interest when the outcome is a commercial product to be sown on tens of millions of hectares, most of which was not encompassed by pre-release testing for trait stability (e.g. GxE).
Kumptia et al (1998) presented a detailed and lucid review of the methods by which genomic integrity is maintained against incursion and/or expression of foreign DNA (and RNA), encompassing the processes of detection, inactivation, and elimination. As a result, as shown by Demeke et al. (1999) in wheat, even when transgenes themselves are stably inherited, the traits they encode may not segregate according to Mendelian ratios. Transgenic constructs can lose their effectiveness within as well as among generations due to a rigorous array of strategies which have evolved to deal with intrusive DNA.
The implications of transgene trait instability are severalfold. Consider first the logistical difficulties introduced into the breeding program itself, when genes can spontaneously "disappear" - literally (if rarely) in the case of excision, or figuratively in the case of silenced expression - in some or all plants in a population. Both trait instability and the randomness of the insertion process itself strongly challenge the purported advantage of genetic engineering in simplifying and accelerating the process of plant breeding. Indeed, the time savings, if any, which may be attributed to applying transgenic means for crop improvement may have been offset by the speed with which these developmentally expensive outcomes have been brought to market. A reduction in the number of site-years of agronomic testing in head-to-head comparison with competing cultivars(3) may have diminished the opportunity to gauge the stability of GE traits over environments (e.g. Myerson, 1997; Coghlen, 1999).
Secondly, for pharmaceutical and industrial applications, transgenic plants must reliably accumulate high levels of target proteins. De Neve et al. (1999) evaluated the stability of antibody (AB) and antibody-binding fragment (Fab) expression in five homozygous lines of transgenic Arabadopsis. In each case, gene silencing occurred, moderating the expression of the transgenes, and hence, introducing instability in AB production. But "each line had a different and specific instability profile", including the proportion of plants affected. Differences in gene silencing apparently arose, in part, due to positional effects - differences among lines in where the transgenes actually inserted. They concluded that "gene silencing phenomena could hamper the general economic exploitation of plants as production systems for heterologous proteins." Thus, not only was gene expression unstable over time, but the instability was unpredictable, depending on where the transgene had inserted.
A related concern would pertain for resistance management strategies for plant pesticidal crops, as Bt corn. As reviewed by Andow and Hutchison (1998), variation in Bt endotoxin concentration in space and time can strongly influence the rate of development of resistance to Bt in target populations. They noted that one of the three preconditions to effective resistance management is that plant tissues must be very toxic, and uniformly so in time and space, to kill all heterozygotes and render resistance a functionally recessive trait. When sufficiently high toxicity is either not expressed or expressed disuniformly, either within an individual plant or a population of plants, or declines below threshold level too early in the season, more heterozygotes survive and rate of resistance greatly accelerates.
The concentration of Bt endotoxin is already known to vary not only among hybrids but among plants within a hybrid, with up to 5% of the plants in an individual field "non-expressing" (perhaps due to gene silencing?). Concentration also varies not only among plant parts, but also declines with time in the season, typically sometime after pollen shed but as late as the end of the season.
Thus, unreliability in expression of transgenic traits is directly damaging to commercially critical processes, not least of which is the efficiency of plant breeding itself, especially for more complex traits. The utility of transgenic crops as bioreactors for industrial uses, and the feasibility of resistance management to plant pesticidal crops are likewise impacted by the inability to reliably sustain transgene function. Yet, as discussed by Kumpatia et al. (1999), instability in transgene function is not only possible but entirely predictable given the plethora of strategies which have evolved specifically for that purpose - to detect, inactivate, and excise alien DNA.
3. Epigenetic Interactions and Unintended Side-Effects. With contemporary understanding of genetics, it seems implausible that anyone could argue that insertion of a transgene would influence only one trait - the target trait - leaving the transgenic crop "substantially equivalent" to conventional crops. Yet this seems to have been the premise that persuaded regulators of the "substantial equivalence" of all 42 of the GE crops now approved for use in Canada.
It is at least arguable that first wave ventures like Roundup resistant crops and Flavr-Saver tomato were agronomically viable primarily because they involved only modifications to existing single genes. Today, however, even industry scientists openly acknowledge the reality of complex, multi-way gene:gene and gene:environment responses to transgene insertion (Kaniewski and Thomas, 1999). The complexity of epistatic and pleiotropic interactions from inserting multiple transgenes seems a formidable challenge to future development in the field.
At issue is the potential for transgene insertions to instigate not simply the target trait, but also unintended secondary outcomes that could pose risks to either the environment or human health. The protocols used to assess risks of transgenic crops in Canada today focus narrowly on only the intended outcomes, virtually ignoring the possibility of unintended outcomes. Evidence presented below challenges the validity of this narrow focus by showing some of the types of unintended side effects which have already been documented for transgenic entities.
Outcrossing. Bergelson et al. (1998) with Arabadopsis thaliana. A. thaliana is a species with a naturally occurring mutant gene conferring chlorosulfuron resistance (Csr1-1). A. thaliana is also a highly selfing species, for which risk of outcrossing is considered negligible (0.3%). Yet when the mutant allele - Csr1-1 was inserted into non-mutant A. thaliana plants, something else changed besides chlorosulfuron resistance. Bergelson et al. (1998) compared the ability of transgenic and mutant (naturally occurring) father plants, each expressing the same Csr1-1 allele, to cross with wild-type plants. Per-plant outcrossing rate was 0.3% for mutant fathers but 6% for transgenic fathers - a roughly 20-fold enhancement. Further studies revealed that transgenic lines differed in their ability to outcross, with rates ranging from 1.2% to 10.8% - or a 4-fold to a 30-fold enhancement in outcrossing.
This study reveals three critical flaws in the process of GE:
Stem Splitting in RR Soybean Coghlan (1999) commented on a study conducted by Bill Vencill of the University of Georgia, where farmers were reporting yield losses in RR soybeans. Losses of up to 40% occurred when RR soybeans were grown in hot spring soils, which not only stunted the plants but also split the stems at first leaf emergence, exposing the plants to pathogen infection. The gene imparting glyphosate tolerance acts at the level of secondary metabolism, thus affecting other metabolic pathways. Among those affected is the phenylalanine pathway, which leads to lignin production, which reportedly can increase by up to 20% in RR soybeans.
Rhizospheric Microbes on Transgenic Alfalfa Giovanni et al. (1999) compared the metabolic fingerprints(4) of soil rhizospheric communities from parental and two transgenic alfalfa cultivars. The transgenic types were developed for industrial enzyme production, having been modified to express either bacterial genes of alpha-amylase or fungal genes for Mn-dependent lignin peroxidase. This combination of parental and two transgenic alfalfas is the model system currently under development by the USEPA to refine the assessment of environmental risks posed by transgenic crops on the rhizosphere and soil microflora. Although isogenic for all but the target enzymes, the metabolic fingerprint of rhizosphere bacterial communities was found to differ, particularly between the parental and the lignin peroxidase alfalfa cultivar. Despite similarities in the metabolic fingerprint of the parental and alpha-amylase transgenic alfalfas, plant genotype-specific differences in bacterial populations were found for each of the three alfalfas. The authors noted that further study is needed to determine if the effects of transgenes on rhizospheric metabolism and species composition in greenhouse-grown plants actually influence field performance of the alfalfa crop or subsequent crops in the rotation.
In sum, genes do not act in isolation, but rather through interactions with other genes. Evidence has been presented to substantiate the concern that inserting a novel transgene can affect unrelated plant traits, and that some unintended effects have persisted through pre-release testing into commercial production. The unintended effects have clear agronomic implications (boll drop and stem splitting) or potential ecological risks (outcrossing and soil bacterial communities). Thus, transgenic crops may differ from conventionally bred crops in more than simply the intended trait, a reality which is not recognized in the risk assessment process used in Canada.
4. Horizontal gene transfer: specifically in the gut Evidence of horizontal gene transfer among unrelated species has been accumulating for at least 20 years, involving such mechanisms as conjugation (cell to cell mating), transduction (transfer helped by viruses), or transformation (direct uptake of DNA by bacteria). According to Ho and Tappeser (1996), a database search of mainstream journals for "horizontal gene transfer" yielded 75 references between 1993 and 1996, of which all but two gave direct or indirect evidence of horizontal gene transfer among quite different bacteria, between fungi, between bacteria and protozoa, between bacteria and higher plants and animals, between fungi and plants, or between insects.
What happens to transgenic DNA when ingested by another organism, say a rat, a cow, or a human? Could the transgenes in Bt potatoes or virus resistant squash survive digestion long enough to transfer horizontally into intestinal microbes, thus radiating antibiotic resistance, viral resistance, or other traits out into unrelated organisms? Or worse, could transgenes even cross over into mammalian intestinal cells, perhaps even transferring traits into our own DNA?
Conventional wisdom had it that DNA is so rapidly digested in the stomach that it is impossible for transgene movement into other organisms to occur, and hence, no risk at all. Next question please. However, evidence challenging this process assumption - as for so many of the assumptions underlying commercial GE crops - has now arisen from several sources.
MacKenzie (1999) reported on a study conducted at Wageningen using an artificial gut designed by Havenaar and colleagues to mimic food digestion. They found that DNA from transgenic bacteria had a half-life of 6 minutes in the large intestine, sufficient time for each bacterium to have a 1 in 10 million change of passing DNA to another bacterium. But with a thousand billion bacteria in a typical gut, many would potentially be transformed with each meal. They further found that up to 10% of the DNA from Flavr Savr tomato survived long enough to reach the colon.
Schubbert and colleagues at the University of Kohn in Germany published a series of papers relating to uptake of transgenic DNA by intestinal and other cells. Using phage M13 amp18 DNA as a test molecule, either pipette-fed or added to the food, they found that 1-2% of the fragments of the test DNA resisted degradation and could be detected hours later in the small intestine, the cecum, the large intestine, and the feces (Schubbert et al., 1997). Fragments of up to 976 bp could also be detected in peripheral leucocytes of the blood 2 to 8 hours after feeding, as well as in the nuclei of spleen and liver cells for up to 24 hours after feeding. In feeding trials of pregnant mice lasting for up to two weeks, transgenic DNA fragments of up to 830 bp moved across the placental barrier and into various organs of both fetal and newborn mice (Schubbert et al., 1998). The DNA was always located in the nuclei of the embryos, but never in all embryonic cells, providing evidence of transplacental rather than germline transmission. The foreign DNA remained in the newborn mice for up to 3 months associated with chromosomes and "probably integrated into host DNA".
From this, Doerfler and Schubbert (1998) concluded that alien DNA is not completely degraded to mononucleotides during digestion, and further, that the intestines are not a barrier to the movement of recombinogenic DNA fragments. Findings based on the naked DNA used in these studies would underestimate the degree to which DNA in transgenic food and feed could persist in the gut. The authors concluded that exposure to undigested DNA fragments via the intestines may be a more common source of infection than foreign genes from viral or microbial vectors.
So, does ingestion of transgenic food constitute a health risk to humans, livestock, or wildlife? The cited studies invalidate the assumption of rapid and complete DNA digestion, but do not address the follow-on question of alien gene insertion and expression via ingested transgenic food. Persistence in the gut is a necessary prerequisite to insertion and expression. If validated by other researchers, this conclusion may encourage consideration of the broader question, to determine if, in fact, a) persistence, insertion, and expression risk is greater in transgenic than in conventional food, and/or b) if it matters.
A simplistic view might wholly discount any risk of insertion of transgenes, as for Bt or glyphosate tolerance, into the human genome. After all, what have these traits to do with us? A wider view might encompass the question raised in (3) above, namely, unpredictable gene interactions initiated by transgene insertion - in this case into the human genome through recombinogenic DNA fragments. Now, it is fair to note that this risk, if it exists at all, may be no different from that posed by recombinogenic DNA from conventionally bred crops. But the particular genes involved are without precedent in human evolution.
Another yet-to-be-considered issue is the scale of exposure to these novel constructs, both to humans and to nature in general. Never before has a diet of corn consisted of every cell containing not only an active endotoxin itself (another issue for another talk), but the genes coding for same. If and when transgenic food constitutes a large fraction of the human diet, with every cell containing one or another of a few novel (alien to human physiology) genetic constructs, exposure and hence risk of horizontal gene transfer will be profoundly increased. The same argument pertains to the exposure risk to nature when tens of millions of hectares of land are sown to a few transgenic crops every year. Even very rare but potentially catastrophic events then become likely instead of implausible, simply due to the scale of exposure.
To recap, then, horizontal gene transfer in the gut could pose a greater risk from transgenic than from conventional food if: a) DNA fragments from transgenic food persist longer in the gut, and have a greater potential to insert themselves into the human genome, and/or b) the inserted transgenes have a greater potential to precipitate secondary gene:gene interactions, with gene products adverse to human health.
2. Real world risks which could have been identified early-on were ignored or missed entirely, due to industry unwillingness to heed the advice of entomologists, ecologists, agronomists, and other real world disciplines. Lawsuits among neighbors over genetic pollution, resistance management refugia which are now prohibitively large with no conclusive evidence they will work, unintended side effects on everything from Monarch butterflies and green lacewings to rhizospheric bacteria, and much more - these are the legacy of a technology prematurely brought to market. The industry has proceeded into a blind alley of its own making, with nowhere to turn.
3. If agricultural GE is going to have a future, it must show how it can shed the burden of inherent process flaws that currently exist. Given what we now know, is it at all realistic to presume that human ingenuity ever will be able to insert genes predictably and stablize trait expression for the complex, multi-genic traits that really matter(5), without engendering other unpredictable and potentially debilitating side-effects?
4. If not now, then when, and at what cost? And in the meantime, how many other promising non-proprietary approaches to achieving the same ends will not be explored, developed, and released, to enhance the productivity, sustainability, and profitability of agriculture - now?
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2. it is recognized that to a scientist (or an engineer), nothing is insurmountable; all problems are potentially soluble if you throw enough money and time at it. As used here, the context is commercially soluble in a way that is both environmentally and societally acceptable now
3. based on a review of industry submissions for GE crops in Canada
4. Based on inoculation of Biolog Gram negative (GN) microplates (96) to generate sole carbon source utilization patterns or metabolic fingerpints; types of bacteria present in each plate (substrate communities) were then compared with ERIC-PCR DNA fingerprinting to identify strains of bacteria
5. e.g. PS rate and photosynthate partitioning, nitrogen fixation, mineral uptake efficiency, drought tolerance, metabolisable energy use efficiency in livestock, and so on?
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