2013 Testimony to Northland Regional Council 21 June 2013

Testimony presented to Northland Regional Council on 21 June 2013 by Dr Peter R Wills, Department of Physics, The University of Auckland.

Expertise

I am a theoretical biologist with 30 years research experience at The University of Auckland, the United States National Institutes of Health and Santa Fe Institute and a large number of research institutes and universities in Germany, most recently the Universität Tübingen. My main area of research concerns the way in which biological systems interpret genetic information. My latest publications in this area are about:

[1]pathological reinterpretation of host genetic information by prion agents;

[2]the fundamental character of genetic information and coding in nature;

[3]biomimetic “genetic coding” control of electronic-chemical nano-particles;

[4]ethical and societal aspects of new biotechnologies.

This research is concerned with the foundations of genetics and the processes responsible for expressing the effects of genetic changes, including those produced by using techniques of genetic engineering (GE). My professional contributions to discussions about genetic engineering include:

[5]commentary for the Bioethics Council;

[6]comprehensive testimony to the Royal Commission on Genetic Modification;

[7]testimony to the Waitangi tribunal;

[8]chapter in a book about GE;

[9]internationally published scholarly work;

[10]authorship of an international scientists’ statement about GE.

In 1987 I was the first researcher ever to use the NZ Official Information Act to gain access to government documents concerning the regulation of genetic engineering activities in New Zealand and I made many submissions to the Environmental Risk Management Authority and the Australia New Zealand Food Authority during the 1990s. I take great care to separate scientific issues from policy issues and value judgments. I likewise take a cautious approach to claims of scientific certainty. I am a founding trustee of Physicians and Scientists for Global Responsibility (New Zealand).

Uncertainty in genetic engineering

Because it is completely impossible accurately to predict the precise effects of making any alteration to the genes of an organism, genetic engineers have to use a trial and error or “suck and see” approach to the evaluation of the changes they make to organisms’ DNA. Having made an alteration to a species, they examine the engineered organism using whatever means are available, including highly specialized biochemical and genetic techniques, to determine how the engineered organism is different from its parent variant. Sometimes the very minutest genetic change, a difference in just one “letter” (of perhaps 3 billion) in the organism’s DNA sequence can significantly alter the characteristics of the organism. This is known from the study of point mutations, like the one in the human hæmoglobin gene that causes sickle cell anæmia and acts as a defence against malaria. Other times, enormous genetic alterations have only minor, perhaps even

imperceptible effects. One can never be completely certain where, on this enormously wide scale, the effects of any particular example of genetic alteration will lie.

Because of this uncertainty, even after the closest laboratory inspection, a genetically engineered organism must be thoroughly tested in its intended environment before scientists can have any confidence in their assessment of how it will perform, either as intended or unintended. This is the purpose of so-called “field trials” that may be permitted by the Environmental Protection Authority (EPA) once they are satisfied that the organism in question has already been adequately studied for its like behaviour to have been reasonably well predicted. However, there is no method known that can, with certainty, determine in advance what the magnitude of the effects of the genetic engineering may turn out to be. Considerable uncertainty always remains, even at the stage of field trials. It is possible for a completely unpredicted effect to turn up unannounced. Furthermore, the magnitude of completely unpredicted effects is also completely unpredictable. A spectacular example of completely unpredicted negative effects turning up at the trial stage, in this case clinical trials of a pharmaceutical GE protein, is provided by the near fatal effects of TeGenero’s TGN1412 when it was administered to 6 people in London in 2006 [11]. The same generic uncertainty besets field trials (or full releases) of genetically engineered crops, trees, animals, insects, micro- organisms, aquatic species etc.

Another important aspect of the EPA process concerns the sources of available information about the genetically engineered organism in question. In most cases the regulatory body must rely almost solely on studies that have been performed by the body wanting to exploit the GE organism, normally for commercial gain. Under these circumstances any scientifically discretionary perspective on the production, selection or presentation of facts has a bias in favour of minimizing the declared potential for harm and the data are likely to have been subject to public relations massaging. However, beyond even that, the proponents of the organism cannot give a complete account of the in situ consequences of the genetic alterations they have effected, let alone consequences arising from introducing the GE organism into a open environment. A vicid illustration of this is the recent discovery by regulators that most common genetic regulatory sequence in commercial GE crops like Roundup Ready soybeans and MON810 maize also encodes a significant fragment of a viral gene that might not be safe for human consumption [12]. The maize recently reported as causing tumours in rats [13] contains the gene fragment.

The difference between genetically engineered species and those found in the natural environment or produced by selective breeding has two sources. The first difference comes from the limited kind of genetic alterations that occur naturally. It is essentially impossible through any sequence of natural events for a gene from a toad in Africa to be transferred to potatoes grown in New Zealand. On the other hand, the artificial creation of such a potato by using the techniques of genetic engineering is a very simple exercise. The second difference comes from the way in which nature acts on genetic variation – evolution through natural selection. This process ensures that genetic variation that leads to catastrophic effects, either on the organism itself or the ecosystem in which it lives, is either weeded out or triumphant over the other species making up the biological environment. As a result of the very long time scale of biological phenomena, decades, centuries, millennia, tens of thousands, millions or billions of years, biological systems have adapted to be relatively safe from most forms of genetic disaster in the medium term, in whatever manner the relevant time scale is defined. The consequences of mutations that occur most readily (and therefore frequently) have long been accommodated into the range of traits of an organism or features of an ecosystem’s robustness. Those less likely in nature are likely to have more severe biological consequences and be subject to harsh natural selection [14].

Thus, most agricultural or ecosystem disasters are caused by climate change, unusual species displacements or the cultivation of maladapted species, not the sudden appearance of new strains of organisms with very unusual genes. (The realm of rapidly mutating viruses is where extreme

phenomena arising from genetic alteration are most often observed.) However, genetic engineering provides the capability of transcending the constraints to which natural sources of potential disaster arising from genetic alterations are subject. In New Zealand the EPA is responsible for ensuring, as far as is practicable and reasonable, that any such risks are adequately mitigated, but the EPA can issue no guarantees. There will always be a residual possibility of harm arising from either intrinsic or extrinsic causes (the genetically engineered organism itself, or unpredictable circumstances, e.g., sabotage), or from lack of compliance with mandatory controls imposed by the EPA. “Lack of compliance” is something of a catchall phrase that can refer to many different processes with consequences for which the responsible body could be liable: executive decisions, staff actions, negligence, corner cutting, errors, system failures, etc. The recent discovery of a GE fungus outside of approved containment facilities at Lincoln University is an example of such an event [15].

GE in Northland

One can imagine commercial interest in a very wide range of proposals for raising, cultivating or culturing genetically engineered organisms in Northland, even at the laboratory or field testing stage of development. The possibilities include:

animals with altered milk or meat characteristics;

animals producing foreign proteins, including human hormones and antibodies; faster growing animals;

animals susceptible to human-like diseases;

pest and herbicide resistant crops – grains, vegetables, fruit, nuts, etc.; plants engineered to grow in extreme environments;

plants with a longer shelf life or with altered size, shape or colour characteristics; faster growing plants;

plants producing foreign proteins;

faster growing or larger fish or crustacea;

fish or crustacea with altered flesh – texture, colour or nutritional characteristics; aquatic species, especially fish or shellfish, engineered to grow in diverse environments;

bacteria, yeast, fungi or algae with intended applications in vinoculture, medicine, brewing, petrochemical industry, environmental restoration, decontamination, biosensing etc.

In advance of details of a specific proposal being disclosed, it is difficult meaningfully to discuss the prospects of harm arising from an activity falling into any of these categories. It is for that reason that a case-by-case approach is taken to the regulation of GE organisms. In regulating laboratory development and field trials of GE organisms in New Zealand, it has been the usual practice of consecutive authorities (the Interim Assessment Group; the Environmental Risk Management Authority; the Environmental Protection Authority) to permit activities to be conducted subject to specific controls. The controls have been devised to mitigate perceived risks, reducing the probability of any harm arising from the activity to some perceived minimum. The question of liability has never been an issue, in fact it was explicitly stated by government that once ERMA had finished its work the risk was “socialized”, i.e., transferred to the community [15].

Precautionary principle and liability

Scientific uncertainty regarding risks of adverse effects are at the heart of the precautionary principle which states (Biodiversity Convention version) that “where there is a threat of significant reduction or loss of biological diversity, lack of full scientific certainty should not be used as a reason for postponing measures to avoid or minimize such a threat” (emphasis added) [16]. A more popular version is given by Wikipedia: “The precautionary principle or precautionary approach states if an action or policy has a suspected risk of causing harm to the public or to the environment, in the absence of scientific consensus that the action or policy is harmful, the burden of proof that it is not harmful falls on those taking an act[ion]” [17].

The amended version of Section 7 (“Precautionary approach”) of the HSNO Act (1996) requires that “All persons exercising functions, powers, and duties under this Act … shall take into account the need for caution in managing adverse effects where there is scientific and technical uncertainty about those effects”. This is much weaker than the obligations imposed by standard versions of the precautionary principle and leaves communities open to greater risks of harm than in jurisdictions where the principle holds proper sway. The essence of the approach is that adverse effects are to be managed, not eliminated. Furthermore, the HSNO Act does not require the question of liability for harm, should it arise later, to be determined at the time of consideration of an application or the imposition of controls. Under such a regime, the determination of liability becomes a complex and expensive legal process occurring after the event and causes further hardship to parties already adversely affected by a breach of controls or safety. Local government has a clear responsibility to protect citizens against such eventualities.

Conclusion

It is my personal judgment that the degree of uncertainty surrounding the extent of harm that could arise from field trials or general releases of GE organisms has not significantly diminished in the quarter century or more during which GE activities have been regulated within New Zealand. For that reason I had no hesitation in joining 50 other international scientists [18] who endorsed the Interim Report of India’s Supreme Court-appointed Technical Expert Committee when it called for a 10-year moratorium on open field trials of Bt crops in India where regulation has been even more inadequate than in our own country.

Recognising: (i) that our EPA is likely to continue granting, with controls, permission for virtually every field trial which is applied for; and

(ii)that the residual risk arising from the possibility of EPA-imposed controls failing or not being complied with is “socialised”, any harm and its cost falling upon the community;

I recommend: that the Northland Regional Council adopt a precautionary approach to the conduct of GE activities within its jurisdiction, including:

(i)the imposition of measures that place full liability upon those who conduct those activities; and

(ii)the fair and wise imposition of additional controls (over and above those imposed by the EPA) that address the specific interests and vulnerabilities of the community in which the activity is proposed, including refusal to allow an EPA-permitted activity to proceed at locations deemed to be unsuitable.

Notes and References

1.Wills P R. Frameshifted Prion Proteins as Pathological Agents: Quantitative Considerations. J. Theor. Biol. 325, 52–61 (2013)

2.Wills P R. Genetic information, mechanical interpreters and thermodynamics; the physico-informatic basis of biosemiosis. Biosemiotics (in preparation, 2013)

3.McCaskill, J S, v. Kiedrowski, G, Oehm, J, Mayr, P, Cronin, L, Willner, I, Herrmann, A, Rasmussen, S, Stepanek, F, Packard, N H, & Wills, P R. Microscale Chemically Reactive Electronic Agents. Int. J. Unconv. Comp. 8, 289–299 (2012)

4.Wills P R, Williams D L F, Trussell D & Mann R. Harnessing our very life. Artificial Life 19 (in press, 2013)

5.Wills P R. The Intrinsic Value of Genes and Organisms, in Reflections on the Use of Human Genes in Other Organisms: Ethical, Spiritual and Cultural Dimensions pp26-30, Toi te Taiao, The Bioethics Council (2004)

6.Wills P R. Testimony to Royal Commission on Genetic Modification, <http://www.gmcommission.govt.nz/publications/PDF_submission.html> (14 November 2000)

7.Wills P R. Testimony to the Waitangi tribunal on behalf of Wai262 claimants (9 May 2002)

8.Wills P R. Disrupting evolution: biotechnology's real result? in Hindmarsh R & Lawrence G Norton J (eds.) Altered Genes pp66-80 (Allen and Unwin) (1998) 2nd Edition, pp53-68 (Scribe Publications, Melbourne) (2001)

9.Wills P R. Correcting evolution: biotechnology’s unfortunate agenda. Revue Internationale de Systémique 8, 455- 468 (1994)

10.Third World Network Concerned Scientists Group. A Statement by Scientists Concerned about Current Trends in the New Biotechnology. The Need for Greater Regulation and Control of Genetic Engineering. pp1-38 (Third World Network, Penang) (1995)

11.Wikipedia. TGN1412. <http://en.wikipedia.org/wiki/TGN1412>

12.Podevin N & du Jardin P. Possible consequences of the overlap between the CaMV 35S promoter regions in plant transformation vectors used and the viral gene VI in transgenic plants. GM Crops and Food 3, 1–5 (2012)

13.Séralini, G-E, Clair E, Mesnage R, Gress S, Defarge N, Malatesta M, Hennequin D & Spiroux de Vendômois J. Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize. Food Chem. Toxicol. (2012)

14.Another feature of GE that is almost always overlooked is the way in which GE changes the rates at which genetic alterations (usually called “mutations”) are made to occur in nature. Evolutionary and ecosystem robustness, change and adaptation can be exquisitely sensitive to the rates at which genetic alterations are introduced into systems, over and above systems’ sensitivity to the substance of the changes. This is more important in relation to highly connected and mutually dependent species in complex ecological networks like ocean or forest environments than it is to monocultures of crop species but it makes clear that the technological application of a “natural” process is not immune from the need for regulation as a form of “genetic modification”. One cannot apply a natural process at a rate thousands of times greater than the normal rate and claim that the outcome.

15.MPI discovers GM fungus at Lincoln < http://www.stuff.co.nz/business/farming/straight- furrow/news/8553485/MPI-discovers-GM-fungus-at-Lincoln> (26 March 2013).

15.I remember being present at a meeting when this was stated by then Environment Minister Simon Upton.

16.Secretariat of the Convention on Biological Diversity. Convention on Biological Diversity. <http://www.cbd.int/iyb/doc/prints/factsheets/iyb-cbd-factsheet-cbd-en.pdf> (Accessed 20 June 2013)

17.Wikipedia. Precautionary principle. <http://en.wikipedia.org/wiki/Precautionary_principle> (Accessed 20 June 2013)

18.Parsai G. Global scientists back 10-year moratorium on field trials of Bt food crops. The Hindu <http://www.thehindu.com/sci-tech/agriculture/global-scientists-back-10year-moratorium-on-field-trials-of-bt- food-crops/article4658619.ece>. (27 April 2013)