GENTECH archive


Re: Bt corn

I do not know if human trials should be really considered, because of the
practical difficulties. I mean, you can not expose humans to a product for
a certain amount of time (and how long should that be?) and than kill them
to see what changes have occured vis-a vis the control group, which also
would have to be killed. To me, studies in the way performed by Dr.
Pusztai (no matter what the Royal Academy of Science is saying) should be
performed, BUT here is where the insanity of the whole story becomes
clear: the pure fact that we need to go through extensive safety trials,
including animal feeding trials, shows how absurd the whole development
is. We have accepted standards of safety where normal (non-GE) crops are
involved. If we now for our food need to go through the kind of testing
mentioned (animals) in a very costly way, what is the sense at all?
Especially in the light of the availability of other techniques in
agriculture which could give the same results as being sought after by
transgenics, but without all the risks and insecurities that GE brings
Wytze de Lange

Roberto Verzola wrote:

> I've been reviewing the safety of Bt corn, due to pending applications
> in the Philippines by two companies (Monsanto and Pioneer) to
> field-test Bt corn here, and in my capacity as NGO representative in
> our National Biosafety Committee.
> I've come across a recent the US EPA paper outlining the various
> safety considerations for Bt corn.
> I am quite surprised at how the EPA concluded that Bt corn is safe for
> human consumption. First, the oral feeding tests were done using NOT
> Bt corn but Bt toxin produced by E.coli. (EPA says that the two are
> "similar.") Second, the tests were done on rats, which showed no
> effects from acute oral feeding. Ergo, according to the EPA, since Bt
> toxin from E.coli is not toxic to rats, therefore, Bt corn does not
> show mammalian toxicity and therefore, it should be safe for human
> consumption.
> I am an electrical engineer, not a genetic engineer, but we use the
> same rules of logic, don't we? All I can say is: it doesn't follow!
> I can see at least four flaws in the EPA reasoning:
> - even if Bt toxin from E.coli is not toxic, it doesn't follow that Bt
> corn is not toxic either; Bt corn must be tested separately
> - even if Bt corn is not toxic to rats, it doesn't follow that it
> is not toxic to other mammals (I haven't seen any feeding studies on
> primates, for example)
> - even if Bt corn is toxic to many mammals, it doesn't follow that it
> is not toxic to humans
> - even if Bt corn is not toxic to humans, it doesn't follow that it is
> safe for human consumption (there are other possible harmful effects
> aside from poisoning)
> My science training tells me that to establish Bt corn's safety for
> human consumption, a controlled experiment that feeds human subjects
> with Bt corn (and not Bt toxin from E.coli) is necessary. Apparently
> this has never been done (or the EPA would have referred to such
> studies), and a recent search also turned up negative results.
> Or I am expecting too much from my fellow engineers of the genetic
> variety?
> Roberto Verzola
> National Committee on Biosafety
> Philippines
> PS. I reproduce a portion of the EPA document below
> Name of Chemical(s): Bacillus thuringiensis CryIA(b) Delta-Endotoxin
> and the Genetic Material Necessary for Its Production in Corn
> Reason for Issuance: Update to Include New Required Refuge Sizes and
> Lifting of Acreage Restrictions in the South
> Date Issued: 730-F-99-004
> ....
> A. Human Health
> 1. Product Analysis - CryIA(b)
> Data were presented which showed that the truncated CryIA(b) toxin can
> be extracted from corn leaf tissue and this purified material displays
> characters and activities similar to that produced in E. coli which
> has been modified to produce CryIA(b). The similarities are shown for
> the tryptic core proteins in molecular weight after SDS-PAGE,
> immunorecognition in Western s and ELISA, partial amino acid sequence
> analysis, lack of glycosylation and bioactivity against either
> European corn borer or corn earworm. This analysis supports the use of
> the microbially produced toxin as an analogue for the plant produced
> protein in mammalian toxicity testing.
> 2. Toxicology Assessment
> There is a reasonable certainty that no harm will result from
> aggregate exposure to the United States population, including infants
> an d children, to the CryIA(b) protein and the genetic material
> necessary for its production. This includes all anticipated dietary
> exposures and all other exposures for which there is reliable
> information.
> The data submitted regarding potential health effects of CryIA(b)
> include information on the characterization of the expressed protein
> in corn, the acute oral toxicity of CryIA(b) , and in vitro
> digestibility studies of the protein. The results of these studies
> were determined applicable to evaluate human risk and the validity,
> completeness, and reliability of the available data from the studies
> were considered. The acute oral toxicity test of bacterially-derived
> CryIA(b) protein showed no test substance related deaths at a dose of
> 4000 mg/kg. This doses represents the highest amounts that could be
> administered with the microbially produced test substances.
> Although CryIA(b) expression level data was required for an
> environmental fate and effects assessment, residue chemistry data were
> not required for a human health effects assessment of the subject
> plant-pesticide ingredients because of the lack of mammalian
> toxicity. Both (1) available information concerning the dietary
> consumption patterns of consumers (and major identifiable subgroups of
> consumers including infants and children) and (2) safety factors
> which, in the opinion of experts qualified by scientific training and
> experience to evaluate the safety of food additives, are generally
> recognized as appropriate for the use of animal experimentation data
> were not evaluated because the lack of mammalian toxicity at high
> levels of exposure demonstrate the safety of the product at levels
> above possible maximum exposure levels. This is similar to the Agency
> position regarding toxicity and the requirement of residue data for
> the microbial Bacillus thuringiensis products from which this
> plant-pesticide was derived. [See 40 CFR Sec. 158.740(b).] For
> microbial products, further toxicity testing to verify the observed
> effects and clarify the source of the effects (Tiers II & III) and
> residue data are triggered by significant acute effects in studies
> such as the mouse oral toxicity study.
> The acute oral toxicity data submitted support the prediction that the
> CryIA(b) protein would be non-toxic to humans. When proteins are
> toxic, they are known to act via acute mechanisms and at very low dose
> levels [Sjoblad, Roy D., et al. "Toxicological Considerations for
> Protein Components of Biological Pesticide Products," Regulatory
> Toxicology and Pharmacology 15, 3-9 (1992 )]. Therefore, since no
> effects were shown to be caused by the plant-pesticide, even at
> relatively high dose levels, the CryIA(b) delta-endotoxin protein is
> not considered toxic.
> Adequate information was submitted to show that the CryIA(b) test
> material derived from microbial cultures were biochemically and,
> functionally similar to the proteins produced by the plant-pesticide
> ingredients in corn. Production of microbially produced protein was
> chosen in order to obtain sufficient material for testing. In
> addition, the in vitro digestibility studies indicate the proteins
> would be rapidly degraded following ingestion.
> The genetic material necessary for the production of the
> plant-pesticide active and inert ingredients are the nucleic acids
> (DNA) which comprise (1) genetic material encoding these proteins and
> (2) their regulatory regions. "Regulatory regions" are the genetic
> material that control the expression of the genetic material encoding
> the proteins, such as promoters, terminators, and enhancers. DNA is
> common to all forms of plant and animal life and the Agency knows of
> no instance where these nucleic acids have been associated with toxic
> effects related to their consumption as a component of food. These
> ubiquitous nucleic acids as they appear in the subject active
> ingredient have been adequately characterized by the applicant.
> Therefore, no mammalian toxicity is anticipated from dietary exposure
> to the genetic material necessary for the production of the subject
> active and inert plant pesticidal ingr edients.
> BPPD has considered available information on the variability of the
> sensitivities of major identifiable subgroups of consumers including
> infants and children and the neurological differences between infants
> and children and adults and the neurological differences between
> infants and children and adults and effects of in utero exposure to
> the plant-pesticides. Since CryIA(b) is a protein, allergenic
> sensitivities were considered. Current scientific knowledge suggests
> that common food allergens tend to be resistant to degradation by
> heat, acid, and proteases, are glycosylated and present at high
> concentrations in the food. Data has been submitted which demonstrates
> that the CryIA(b) delta-endotoxin is rapidly degraded by gastric fluid
> in vitro and is non-glycosylated. Studies submitted to EPA done in
> laboratory animals have not indicated any potential for allergic
> reactions to B. thuringiensis or its components, including the
> delta-endotoxin in the crystal protein. Despite decades of widespread
> use of Bacillus thuringiensis as a pesticide (it has been registered
> since 1961), there have been no confirmed reports of immediate or
> delayed allergic reactions to the delta-endotoxin itself despite
> significant oral, dermal and inhalation exposure to the microbial
> product. Several reports under FIFRA  6(a)2 have been made for
> various Bacillus thuringiensis products claiming allergic reactions.
> However, the Agency determined these reactions were not due to
> Bacillus thuringiensis itself or any of the Cry toxins. Thus, the
> potential for the CryIA(b) protein to be a food allergen is minimal.
> BPPD has considered available information on the cumulative effects of
> such residues and other substances that have a common mechanism of
> toxicity. These considerations included the cumulative effects on
> infants and children of such residues and other substances with a
> common mechanism of toxicity. Consideration of a common mode of
> toxicity is not appropriate given that there is no indication of
> mammalian toxicity of the plant-pesticides and no information that
> indicates that toxic effects would be cumulative with any other
> compounds.
> BPPD has considered available information on the aggregate exposure
> levels of consumers (and major identifiable subgroups of consumers) to
> the pesticide chemical residue and to other related substances. These
> considerations include dietary exposure under the tolerance exemption
> and all other tolerances or exemptions in effect for the
> plant-pesticide chemical residue, and exposure from non-occupational
> sources. Exposure via the skin or inhalation is not likely since the
> plant-pesticides are contained within plant cells which essentially
> eliminates these exposure routes or reduces these exposure routes to
> negligible. Oral exposure, at very low levels, may occur from
> ingestion of processed corn products and drinking water. However a
> lack of mammalian toxicity and the digestibility of the
> plant-pesticides has been demonstrated. The use sites for CryIA(b)
> delta endotoxin are all agricult ural for control of lepidopteran
> insects. Therefore, exposure via residential or lawn use to infants
> and children is not expected.
> BPPD has considered available information on whether the
> plant-pesticides may have an effect in humans that is similar to an
> effect produced by a naturally occurring estrogen or other endocrine
> effects. The active ingredient is a protein plant-pesticide derived
> from the microorganism Bacillus thuringiensis. No known metabolite
> that acts as an "endocrine disrupter" is produced by this
> microorganism. Therefore, no adverse effects to the endocrine system
> is known or expected.
> 3. Tolerance Exemption Conclusions
> The Agency has concluded that establishment of a tolerance is not
> necessary to protect the public health and established an exemption
> from tolerance requirements for the active ingredient in this product
> on 8/2/96 as set forth below. This exemption remains in effect
> pursuant to FFDCA section 408(j)(3).
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