It categorically is an inderect safety study. Not as powerful perhaps as a study designed specifically around safety, but a toxic/unsafe substance in the feed would most certainly effect the various growth parameters.

Taking a bit of a better look around I came across this passage:-

Monsanto Canada Inc. has submitted data from dietary toxicity studies on the effect of Cry1A.105 or Cry2Ab2 protein on non-target invertebrates, including the honeybee larvae and adult (Apis mellifera), minute pirate bug (Orius insidiosus), ladybird beetle (Coleomegilla maculata), a parasitic wasp (Ichneumon promissorius), and earthworm (Eisenia foetida). Collembola (Folsomia candida) were fed an artificial diet containing 50% of MON 89034 leaf tissue. In all cases, the Cry1A.105 and Cry2Ab2 proteins were demonstrated to be safe to these indicator species at doses equal to or exceeding 14 times the estimated environmental concentration of Cry1A.105 and Cry2Ab2 proteins in the diet of non-target invertebrates feeding on MON 89034 tissues or exposed to MON 89034 corn via their preys. In addition, no adverse effects were observed when the aquatic invertebrate Daphnia magna was exposed to MON 89034 corn pollen at a concentration of 100 mg/L, which indicates that no hazard is anticipated to aquatic invertebrates from exposure to MON 89034 corn pollen.

Data was also submitted on non-target vertebrates including the mouse, the bobwhite quail and broiler chicken. No adverse effects were detected when mice were exposed to a single oral dose of 2,072 mg Cry1A.105 protein/kg body weight or 2,198 mg Cry2Ab2 protein /kg body weight. These doses represent several thousand times the worst-case daily dose of Cry1A.105 and Cry2Ab2 proteins to humans or livestock feeding on MON 89034 grain. No adverse effects were detected when bobwhite quail or broiler chicken were fed a diet containing 50% MON 89034 corn grain for 8 days and 42 days, respectively.

In

http://www.inspection.gc.ca/english/plaveg/bio/dd/dd0874e.shtml#a11

which a) shows there is more data available, at least to the regulatory bodies (acceptance by a regulatory body is a form of peer review, as the regulatory scientists can be considered peers – ideally though it would be nice if this data were also peer reviewed in a publically available scientific journal (it may be and my ability to find it may be the issue))
b) shows that regulatory bodies do consider broiler studies as a form of safety study.

August 17, 2009 at 8:40 am
I’ll concede that no, the broiler study isnt directly a safety study, and that on a second look I’m not having much luck finding published info on the Cry1A.105 protein (I did find a safety level quoted for it in one paper, but unfortunately the reference was to unpublished research by Monsanto) –
++++++++++++++++++=
It’s not even indirectly or anything close to a safety study and you should know that. Are there any real safety studies? If not, how does this get approved?

Earlier on the blog we have addressed our stance on labeling, found here. You can also find it on our For the Record page of Monsanto.com.

Maybe you really believe in what you say. I really don’t understand one thing.. Why is Monsanto insistent on cumbersome FDA labeling for GM foods, when it is my fundamental right to put only what I wish in my body? If Monsanto really believes in what they say why not proudly emblazon GM modified right across the packet? Perhaps it is because Monsanto’s track record is nothing to be inspired by….it was the same company that claimed in the 1960s that Agent Orange did not have any effect other than defoliating trees!

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/Ames_Causes.html

(following your link to a nice logical conclusion) also undermines to a certain extent the validity of positive Ames tests in making any kind of safety decisions, and, in an unrelated note, gives a good authoritative statement around fears of pesticide residue toxicity compared to lack of fears around a single cup of coffee. (so thanks for that, not a comparison I’d come across before)

On number 4 again – you state as ‘fact’ that these proteins from plants and bacteria differ and that this is an issue – what evidence of difference do you have beyond a concern that there may be a difference? I still think it logically holds that if the proteins still work in the way that the bacterial protein works, and the coding regions are the same (in terms of amino acids, at a guess there may be some codon differences to achieve proper expression in plants) then the proteins themselves will also be the same (working on the assumption that modifications made by the plant to the protein would reduce or eliminate efficacy of the protein)

What are the differences you are proposing? Why would you believe that these differences would then end up being harmful rather than either doing utterly nothing, or simply reducing or eliminating protein function.

I’ll concede that no, the broiler study isnt directly a safety study, and that on a second look I’m not having much luck finding published info on the Cry1A.105 protein (I did find a safety level quoted for it in one paper, but unfortunately the reference was to unpublished research by Monsanto) – I still believe that the broiler study can be considered as a safety study to a certain extent (I think this came up in another posting in which Dr.Dan (I think…) explained the utility of broiler studies in looking at feed safety) although clearly not first choice.

I’m also somewhat confused by your statement about a lack of scientific vision. Unless you’re defining scientific vision as seeing boogeymen under the bed and harm in everything we haven’t tested under every condition we can imagine. My coverage of the points was intended to address the points from a somewhat scientific stance (at least utilizing current scientific knowledge combined with a little logic – not exactly the scientific method at work, but good enough for a debate on the points I feel – or does only one side of the arguement get to attempt this style of debating?)

August 11, 2009 at 2:42 pm

7. As all the transproteins (as far as I know) are sourced from bacteria it seems to me that testing for mutagenicity is somewhat an odd request, why would bacteria express mutagenic (to themselves) proteins
****************

I believe what the Austrian Ministry of Health is referring to in this point:

“7. Moreover it is suggested to carry out mutagenicity tests on bacteria with the
transproteins.”

is an Ames Test–The Health Ministry is not concerned that the proteins would be mutagenic to the bacteria producing them in Nature. It is people and animals about whom and which they are concerned: http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/A/AmesTest.html

“The use of the Ames test is based on the assumption that any substance that is mutagenic (for the bacteria used in his test) may also turn out to be a carcinogen; that is, to cause cancer.”

This is standard safety screening testing.

“Both studies were conducted to compare bird performance (feed intake, BW,and adjusted feed:gain), carcass yield, and meat quality
of the birds fed the diets containing the test corn, control corn (genetic background similar to the test corn), and conventional corn.”

This is not how a safety study is conducted. Safety is not measured by carcass yield and meat quality.

2. – http://ps.fass.org/cgi/reprint/86/9/1972
or http://ps.fass.org/cgi/content/abstract/86/9/1972
if the full article isnt publicly available

Shows a safety study with the Cry1A.105 protein – I assume the arguement being made is that there is no history of safety in terms of comparison to the other Bt proteins which have proven safe used in organic ag, and in transgenics since their release (that or the author cant do a spectacularly simple search)

3. If true then surely 2 is pointless? I dont agree with the assertion, the mode of action of the proteins is the same whether sprayed or inserted into the plant, the safety of one gives a pretty good guarantee of the safety of the other.

4. I’d personally guess that as the proteins are initially microbial, and work in plants, that the structure cannot be overly dissimilar (if plants altered the structure to a great degree the proteins would cease working)

6. I dont see a credible reason to believe the proteins produced would interact synergistically or alter metabolite profiles of the transgenic plants in any significant way – the enzymes introduced are well characterized and serve the same function as the enzyme which the herbicide knocks out – as such I see no reason to suppose some additional as yet uncharacterized function. The insecticidal proteins are non-enzymatic, therefore I cant see a massive cause for concern in changes in metabolite levels, and interactions with other proteins in the plant proteome seem unlikely due to the high specificity proteins require to interact in a meaningful way – considering the evolutionary distance between the source organism and the plant it is unlikely that such specific interactions would exist.

7. As all the transproteins (as far as I know) are sourced from bacteria it seems to me that testing for mutagenicity is somewhat an odd request, why would bacteria express mutagenic (to themselves) proteins.

8. Equally then there is no proof of safety of any crop grown. I’m pretty confident that if any real effect was there that it would have been observed and tested by now.

Hmm… that appears to be somewhat more than a couple… anyway hopefully someone with a little bit more expertise can come in and give a somewhat more official stance on these.