Fwd: GMW:_Prof_Terje_Traavik_in_his_own_words

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GMW:_Prof_Terje_Traavik_in_his_own_words

" GM_WATCH "

Fri, 19 Mar 2004 20:22:44 GMT

 

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Below is an important statement from Prof Terje Traavik, the text of which is

reproduced in full from a pdf which can be sent to anyone who would prefer to

receive it in its original format.

 

First some introductory comments from Dr Ignacio Chapela from whom we received

this.

 

(For more statements about GM by scientists see:

http://www.gmwatch.org/p1temp.asp?pid=3 & page=1)

---

Dear colleagues,

 

Perhaps some of you did not register the recent

flare of internet news and counternews

epicentered from Kuala-Lumpur. Following a

presentation by Terje Traavik to the forum of

scientists, regulators, civic groups and individuals gathered for the

Biodiversity Convention meetings, we were all bracing for a new round of the now

common pattern of (a) scientific news followed by (b) discredit, followed by ©

silence, followed by (d) business-as-unusual as always these days (cf the first

seven minutes of the webcast

http://nature.berkeley.edu/pulseofscience).

 

Not this time. I want to share with those who

might not have received it, a document which is

perhaps the most important science writing in the

last quarter century - a span of time convenient

to my ignorant mind since it matches the rough

age of the Bioteck Rev.

 

I invite you to read Terje's own words, which

carry the pregnancy of our dire times seen

through the transparent lens of Tromsø, 70

degrees N Latitude. If nothing else, I expect we

will all be engaged with this document for years

to come, in its own way a break of silence.

 

Of course it is not a coincidence that these words would be coming to us in

tandem with Bruno Latour's own retraction of sorts, his spitting at

" critical barbarity " , his call to move from matters-of-fact to

matters-of-concern (cf Critical Inquiry, or better edited, Harper's).

 

Bruno tracking Terje?

 

With regards,

Ignacio

---

A response to criticism about our work on GE biosafety.

 

The Cartagena protocol, the Precautionary principle, " sound science " and " early

warnings " .

 

Terje Traavik, Dr. philos.

Scientific Director, GENØK-Norwegian Institute of Gene Ecology

Professor of Gene Ecology, University of Tromso

 

Background

 

On February 22, 2004, I presented the results of ongoing research at the

Biosafety Symposium in Kuala Lumpur, held just prior to the first Meeting of the

Parties on the Cartagena Protocol on Biosafety. The Symposium was jointly

organised by the Third

World Network (a science-interested organisation), the Norwegian Institute of

Gene Ecology (GENØK) and the New Zealand Institute of Gene Ecology.

 

The Symposium was accessible to the public, but it was primarily a meeting for

those with professional interests in biosafety.

 

The presentation of our preliminary research findings was done in the spirit of

the greatest of traditions to share the results of research among peers. This

tradition has dominated the biological sciences for centuries. Possibly that

tradition has become difficult to recognise in an age when most research is

filtered for information that must be kept secret for commercial or other

reasons. I am proud and grateful to be supported by public agencies who impose

no such requirements.

 

Speaking now for the two Institutes of Gene Ecology, we also reject any

inclination among particular parties to define our peer group. The Institutes of

Gene Ecology are organised on the principle that bio-applications will have

impacts on the planet and the ecology of human beings that transcend dated and

arbitrary notions of where biology ends and ethics, social science, law,

economics, philosophy and culture begin. Our peer group is composed of those who

are specialists in the impacts of genetically engineered organisms.

 

As a community we have a membership that covers all traditional research

backgrounds mentioned above. More importantly, each individual among us has a

commitment to understand what can be learned from all those disciplines when

focused on a single issue - genetically engineered organisms.

 

That latter quality opens our minds to the bodies of

knowledge held in non-traditional sources. By this we mean both NGOs and the

industry. Our peer group and our emerging competence in holistic impact

assessment is what we believe make us unique.

 

I have been criticised for speaking about my research at the Kuala Lumpur

Biosafety Symposium. This is an insult to the audience which was composed of

respected scientific specialists, members of the competent regulatory community,

and accomplished researchers of the many disciplines whose interests intersect

the impacts of new bioapplications, including genetically engineered organisms.

 

Cartagena Protocol

 

The Precautionary Principle plays an important role in the Cartagena Protocol,

an international agreement on transboundary movement of GMOs

(www.biodiv.org/biosafe/protocol), and in regulations, i.e. the Norwegian Gene

Technology Act of 1993 (www.bion.no) and EU directive

2001/18/EC(www.europa.eu.int/comm/food/fs/sc/scp/out31_en.html). The

Precautionary Principle instructs us to anticipate the potential hazards of

genetic engineering applications.

 

Employment of the Precautionary Principle (PP) entails identification of risk,

scientific uncertainty and ignorance, and involves transparent and inclusive

decision-making processes (Freestone and Hey, 1996). Although a tool for policy

decision, I will claim that implementation of the PP must have impact on the

research agenda. Employment of the PP emphasises the importance of scientists

taking responsibility for anticipation, acknowledgement and communication of

uncertainty, in order to produce scientifically and socially robust knowledge

(Myhr and Traavik, 2003).

 

In a very real sense, the spirit of Cartagena, perhaps uniquely, gives the

environment legal

standing and places the burden-of-proof of safety on those who might damage her.

I favour application of a strong version of the PP, realizing the need to

identify and acknowledge scientific uncertainty related to GE applications

before they are commercialised. The future of mankind and the environment is

inter-dependent. Damage to ecosystems and other species will also hurt mankind

in the long run. Pure anthropocentric world views may be suicidal for the human

species.

 

When I agreed to speak at the Biosafety Symposium, I fully understood the

ethical

dilemmas facing scientists when potential " early warnings " of harm to health and

the environment appear in their own research. Raised a traditionalist, I began

my talk by stating my respect for peer-review as an integrated and necessary

part of " sound science " and I of course believe in it. In fact, I believe in it

so strongly that I have always, and intend to always, place my work before the

entire world, not just before the competent regulatory authorities with

restrictions on discussing the content of my findings. This

includes early warning reporting. Such reports are necessary to inform other

scientists and regulators, giving them the opportunity to " anticipate and

prevent " , and should be followed up by further research to reveal the validity

of the warnings

(reports.eea.eu.int/environmental_issue_report_2001_22/).

 

Peer review itself does not make a scientific finding either true or false. Peer

review is neither a single event. Many peer-reviewed publications include the

results of research previously tested in a seminar or conference before a

critical audience, and before that in a grant application. Grant applications

also often contain summaries of preliminary findings.

This provides some confidence to granting agencies and their reviewers. The

critical audiences alerted to your work during seminars may also begin the

process of being inspired to reproduce or extend your findings in ways your

imagination has not even

considered. That is the process we foster in the professional community; not the

process of

secrecy.

 

When it comes to the environment and human health, I strive for nothing less

than the most

stringently conducted and reported science. That standard is not compromised

because some warnings of potential hazard are notified to the competent

community through the means discussed above, and early warnings do not preclude

the work being subjected to further review as it progresses through to eventual

publication in a peer-reviewed journal, often many months in the future.

 

By similar token, early insight into the commercialisation potential of a

research finding

would also not await publication in a peer-reviewed journal before a patent

application was lodged. The patent is therefore based on observations and tests

that have never been openly reviewed, yet applications protected by patents are

no less prone to cause concern among the public and governments.

 

What was the research presented in Kuala Lumpur?

In my talk, in order to illustrate what I meant by " early warnings " , I very

briefly summarized results from three on-going, long-term projects at GENØK:

 

*Feeding experiments in rats

*Antibody analyses of sera from Philippine farmers

*Safety aspects of transgenic poxvirus-vectored vaccines

 

The second item, sera from farmers, has attracted the greatest interest so I

will briefly summarise those findings below.

 

We have used direct and inhibitory ELISAs (enzyme-linked immuno-sorbent assays)

to demonstrate IgA, IgG and IgM antibodies specifically binding to Bt-toxin

Cry1Ab in sera from Philippine farmers. A general interpretation would be that

the farmers had been exposed, in an immunologically meaningful way, to Cry1Ab,

or an antigen sharing epitopes with Cry1Ab, during the last 6-9 months before

blood samples were taken. This might indicate coincidence in time between three

observed events: the very first pollination season for Bt-transgenic maize, an

outbreak of respiratory/intestinal disease among individuals living close to the

Bt-maize field, and the production of serum antibodies.

 

I strongly emphasized that the tests could not establish any cause-effect

relationships between the 3 events, neither could the results preclude such

relationships, and hence they might represent an early warning. As I said at the

time, even if I had been able to present the detection of specific anti-Cry1Ab

IgE antibodies, my conclusions would have been the same.

 

Why have these results, among many thousands of scientific results presented at

conferences annually, attracted so much attention?

 

These results could challenge long-standing claims based on many unpublished or

not peer-reviewed research conducted over the years.

 

1. *Cry1Ab is not immunogenic*. The bacterial version of Cry1Ac shares antigenic

'epitopes' with Cry1Ab. Since Cry1Ac is strongly immunogenic in rodents, a fact

backed up by a series of peer-reviewed articles (e.g. Moreno-Fierros et al 2002;

Vazquez et al. 1999, Vazquez-Padron et al., 2000), it is a fair hypothesis that

Cry1Ab could inspire an immunological response. Also, Bacillus thuringiensis

spraying has elicited specific Cry1A antibodies in farm workers, within the same

classes we detected, as well as allergy-related IgE antibodies. These findings

were published already in 1999 (Bernstein et al., 1999). There is a distinct

difference between being " allergenic " and " antigenic " / " immunogenic " : all that is

immunogenic is not allergenic.

 

However, immunogens invoke an immune response and any immune response should be

further investigated for being indicative of a potential allergic response.

 

I am aware of no evidence in the existing peer-reviewed literature that

demonstrates that these proteins are neither allergenic nor immunogenic. I am

aware of claims that the linear amino acid sequence of the Cry proteins is not

similar to any known allergens, but this again is controversial (i.e. Kleter and

Peijnenburg, 2002)

 

Furthermore, that type of evidence has never been evaluated as predictive of

proteins that will turn out to not be allergens (Metcalfe, 1996; Stickler et al.

2003).

 

Moreover, the engineered plant versions of Cry proteins are C-terminally

truncated compared to the bacterial protoxins. New epitopes may be created in

plants due to new alternative posttranslational modifications and folding of the

protein, or on the basis of complexing between the transgene product and

endogenous protein(s).

 

Indeed, most antibodies produced by an allergic individual to inhalant allergens

appear to be toward discontinuous epitopes, but it is unknown whether this

applies to antibodies to food allergens (Taylor and Lehrer, 1996). These are

" sound " scientific hypotheses yet to be experimentally tested, which they should

have been before commercialisation of Bt-transgenic plants.

 

2. *Pollen does not express the cry1ab gene*. This may be true, but if it is it

needs to be verified rigorously. By that I mean it must be measured in all

engineered plants, it must be measured in plants grown at all sites, and it must

be measured for plants grown under different physiological conditions, for a

start. The claim should also

be made only after corroboration via a number of complementary techniques, e.g.

antibody screening of pollen and microarray analysis. This is because eukaryotic

promoters, in this case the 35S CaMV promoter used to drive the expression of

the gene, can be inactive in one specific environment, for instance somewhere in

the US, but there is not absolute reason for it to not be activated in other

environments.

 

To my knowledge, there are no data proving promoter silence in pollen of any

Bttransgenic

maize variety, and some data to the contrary. For example, for MON 810 corn

grown in the U.S., the concentration of Cry was low but detectable (< 90ng/g

total protein) (U.S. EPA Bt crop reassessment data).

 

How much is too little to inspire an allergic reaction? There is currently no

lower threshold for sensitization to allergens as far as I know, and certainly

not food allergens, although very low concentrations make sensitization less

likely .

Furthermore, when Bt crops were assessed for allergenicity by the US, they were

not carried out according to the best recommended methods (FAO/WHO), undermining

confidence in that evidence. The regulatory assessment also assumed

sensitization only via oral exposure, not possible respiratory exposure.

 

Conclusion

 

The Biosafety Protocol's main objective is to regulate the trans-boundary

movement of

genetically engineered organisms for purposes of protecting human and

environmental health. In the spirit of the Protocol, that capacity must be

relevant to the special or unique concerns of the importing nations and their

environments.

 

It is broadly recognized that third world nations are a huge global repository

of biodiversity, local knowledge and cultural treasures, much of it yet to be

described. Since at present most genetically engineered organisms originate in

the first world nations, their movement to other ecosystems must proceed only

with the consent of the fully informed

citizenry of these nations. With yet-to-be determined impacts of genetically

engineered

organisms on biodiversity and human health, many species as well as cultures

could be at risk from international movements of these organisms. In addition,

since most genetically engineered organisms are imported along with first world

co-technologies (such as certain agricultural practices, pesticides, herbicides,

etc.), trans-boundary movement of genetically engineered organisms could

threaten various cultures.

 

Astute observers of genetically engineered organisms cannot help but recognize

that the

limitations of biosafety infrastructure are not limited to third world

countries, but are a result of a global under-investment in science-for-safety.

In this regard, the two Institutes of Gene Ecology are optimistic that this is

only the beginning of a sustained effort to raise global awareness and capacity

in biosafety. In fact, that biosafety is the priority of the third world is an

interesting testimony to the fact that priority investment in science-for-sale

does not suit all cultures and is exposing significant gaps even among wealthy

nations.

 

Norway should also be proud that it has taken a leadership position in

championing and resourcing the call for science-for-safety as the world's newest

priority.

 

Literature cited

Bernstein, I.L, Bernstein, J.A., Miller, M., Tierzieva, S. et al. 1999. Immune

responses in farm workers after exposure to Bacillus thuringiensis pesticides.

Environmental Health Perspectives 107: 575-582

 

CBD: Cartagena Protocol on Biosafety ( http://www.biodiv.org/biosafe/protocol)

 

EEA: European Environment Agency (2002): Late lessons from early warnings. The

precautionary

principle 1896-2000

(http://reports.eea.eu.int/environmental_issue_report_2001_22/)

 

European Council Directive 2001/18/EC

(http://www.europa.eu.int/commm/food/fs/sc/scp/out31_en.html

 

Freestone, D. and Hey, E. (1996): Origins and development of the precautionary

principle, in

Freestone, D. and Hey, E. (ed.), The precautionary principle and international

law (Netherlands:

Kluwer Law International), p.3-15.

 

Gene Technology Act 1993. The act relating to the production and use of

genetically modified organisms. Act no. 38 of 2 April 1993, Oslo.

http://www.bion.no/biotech_regulations_eng.shtml

 

Kleter, G.A. and Peijnenburg, AACM. 2002. Screening of transgenic proteins

expressed in

transgenic food crops for the presence of short amino acid sequences identical

to potential

IgE-binding linear epitopes of allergens. BMC Structural Biology 2:8

 

Metcalfe, D.D., J.D. Astwood, R. Townsend et al. 1996. Assessment of the

allergenic potential of foods derived from genetically engineered crop plants.

Crit. Rev. Food Sci. Nutr. 36(S): S165–S186.

 

Moreno-Fierros, L., Garcia, N., Lopez-Revilla, R., Vazquez-Padron, R.I. 2000.

Intranasal, rectal and intraperitoneal immunization with protoxin Cry1Ac from

Bacillus thuringiensis induces compartmentalized serum, intestinal, vaginal and

pulmonary immune responses in Balb/c mice. Microbes and Infection 2: 885-890

 

Myhr, A.I., Traavik, T., 2003. Genetically modified crops: Precautionary science

and conflicts of interests. JAGE 16, 227-247.

 

Stickler M., Much, J., Estell, D., Power, S., Harding, F. 2003. A human

dendritic cellbased method to identify CD4+ T-cell epitopes in potential protein

allergens. Environmental Health Perspectives 111: 251-254

 

Taylor, S.L., S.B. Lehrer. 1996. Principles and characteristics of food

allergens. Crit. Rev.

Food Sci. Nutr. 36(S): S91–S118.

 

Vazquez, R.I., Moreno-Fierros, L., Neri-Bazan, L., de la Riva, G.A. 1999.

Bacillus thuringiensis Cry1Ac protoxin is a potent systemic and mucosal

adjuvant. Scand J. Immunol. 49: 578-584

 

Vazquez-Padron, R.I., Moreno-Fierros, L., Neri-Bazan, L., et al. 2000.

Characterization of

mucosal and systemic immune response induced by Cry1Ac protein from Bacillus

thuringiensis HD 73 in mice. Braz. J. Med. Biol. Res. 33: 147-155

 

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