Spilling the Beans, May 2006

Genetically Engineered Crops May Produce Herbicide Inside Our Intestines

By Jeffrey M. Smith

Pioneer Hi-Bred's website boasts that their genetically modified (GM)
Liberty Link[1] corn survives doses of Liberty herbicide, which would
normally kill corn. The reason, they say, is that the herbicide becomes
"inactive in the corn plant."[2] They fail to reveal, however, that after
you eat the GM corn, some inactive herbicide may become reactivated inside
your gut and cause a toxic reaction. In addition, a gene that was inserted
into the corn might transfer into the DNA of your gut bacteria, producing
long-term effects. These are just a couple of the many potential
side-effects of GM crops that critics say put the public at risk.

Herbicide tolerance (HT) is one of two basic traits common to nearly all GM
crops. About 71% of the crops are engineered to resist herbicide, including
Liberty (glufosinate ammonium) and Roundup[3] (glyphosate).  About 18%
produce their own pesticide. And 11% do both. The four major GM crops are
soy, corn, cotton and canola, all of which have approved Liberty- and
Roundup-tolerant varieties. Herbicide tolerant (HT) crops are a particularly
big money-maker for biotech companies, because when farmers buy HT seeds,
they are required to purchase the companies' brand of herbicide as well. In
addition, HT crops dramatically increase the use of herbicide,[4] which
further contributes to the companies' bottom line.

There are no required safety tests for HT crops in the US-if the biotech
companies declare them fit for human consumption, the FDA has no further
questions. But many scientists and consumers remain concerned, and the
Liberty Link varieties pose unique risks.

Liberty herbicide (also marketed as Basta, Ignite, Rely, Finale and
Challenge) can kill a wide variety of plants. It can also kill bacteria,[5]
fungi[6] and insects,[7] and has toxic effects on humans and animals.[8] The
herbicide is derived from a natural antibiotic, which is produced by two
strains of a soil bacterium. In order that the bacteria are not killed by
the antibiotic that they themselv es create, the strains also produce
specialized enzymes which transform the antibiotic to a non-toxic form
called NAG (N-acetyl-L-glufosinate). The specialized enzymes are called the
pat protein and the bar protein, which are produced by the pat gene and the
bar gene, respectively. The two genes are inserted into the DNA of GM crops,
where they produce the enzymes in every cell. When the plant is sprayed,
Liberty's solvents and surfactants transport glufosinate ammonium throughout
the plant, where the enzymes convert it primarily into NAG. Thus, the GM
plant detoxifies the herbicide and lives, while the surrounding weeds die.

The problem is that the NAG, which is not naturally present in plants,
remains there and accumulates with every subsequent spray. Thus, when we eat
these GM crops, we consume NAG. Once the NAG is inside our digestive system,
some of it may be re-transformed back into the toxic herbicide. In rats fed
NAG, for example, 10% of it was converted back to glufosinate by the time it
was excreted in the feces.[9] Another rat study found a 1% conversion.[10]
And with goats, more than one-third of what was excreted had turned into
glufosinate.[11]

It is believed that gut bacteria, primarily found in the colon or rectum,
are responsible for this re-toxification.[12] Although these parts of the
gut do not absorb as many nutrients as other sections, rats fed NAG did show
toxic effects. This indicates that the herbicide had been regenerated, was
biologically active, and had been assimilated by the rats.[13] A goat study
also confirmed that some of the herbicide regenerated from NAG ended up in
the kidneys, liver, muscle, fat and milk.[14]

More information about the impact of this conversion is presumably found in
"Toxicology and Metabolism Studies" on NAG, submitted to European regulators
by AgrEvo (now Bayer CropScience). These unpublished studies were part of
the application seeking approval of herbicide-tolerant canola. When the UK
government's Pesticide Safety Directorate attempted to provide some of this
information to an independent researcher, they were blocked by the company's
threats of legal action.[15] The studies remained private.

Toxicity of the herbicide

Glufosinate ammonium is structurally similar to a natural amino acid called
glutamic acid, which can stimulate the central nervous system and, in excess
levels, cause the death of nerve cells in the brain.[16] The common
reactions to glufosinate poisoning in humans include unconsciousness,
respiratory distress and convulsions. One study also linked the herbicide
with a kidney disorder.[17] These reactions typically involve large amounts
of the herbicide. It is unclear if the amount converted from GM crops would
accumulate to promote such responses or if there are low dose chronic
effects.

Perhaps a more critical question may be whether infants or fetuses are
impacted with smaller doses. A January 2006 report issued by the
Environmental Protection Agency's (EPA) Office of Inspector General said
that studies demonstrate that certain pesticides easily enter the brain of
young children and fetuses, and can destroy cells. That same report,
however, stated that the EPA lacks standard evaluation protocols for
measuring the toxicity of pesticides on developing nervous systems.[18]
Scientists at the agency also charged that "risk assessments cannot state
with confidence the degree to which any exposure of a fetus, infant or child
to a pesticide will or will not adversely affect their neurological
development." [19] Furthermore, three trade unions representing 9,000 EPA
workers claimed that the evaluation techniques used at the agency were
highly politicized. According to a May 24, 2006 letter to the EPA's
administrator, the unions cited "political pressure exerted by Agency
officials perceived to be too closely aligned with the pesticide industry
and former EPA officials now representing the pesticide and agricultural
community."[20]

Although the EPA may be hampered in its evaluations, research has
nonetheless accumulated which suggests that glufosinate carries significant
risks for the next generation. According to Yoichiro Kuroda, the principal
investigator in the Japanese project entitled "Effects of Endocrine
Disrupters on the Developing Brain," glufosinate is like a "mock
neurotransmitter." Exposure of a baby or embryo can affect behavior, because
the chemical disturbs gene functions that regulate brain development.[21]

When mouse embryos were exposed to glufosinate, it resulted in growth
retardation, increased death rates, incomplete development of the forebrain
and cleft lips,[22] as well as cell death in part of the brain.[23] After
pregnant rats were injected with glufosinate, the number of glutamate
receptors in the brains of the offspring appeared to be reduced.[24] When
infant rats were exposed to low doses of glufosinate, some of their brain
receptors appeared to change as well.  <> [25]

Glufosinate herbicide might also influence behavior. According to Kuroda,
"female rats born from mothers that were given high doses of glufosinate
became aggressive and started to bite each other-in some cases until one
died." He added, "That report sent a chill through me."[26]

Disturbing gut bacteria

If the herbicide is regenerated inside our gut, since it is an antibiotic,
it will likely kill gut bacteria. Gut microorganisms are crucial for health.
They not only provide essential metabolites like certain vitamins and short
fatty acids, but also help the break down and absorption of food and protect
against pathogens. Disrupting the balance of gut bacteria can cause a wide
range of problems. According to molecular geneticist Ricarda Steinbrecher,
"the data obtained strongly suggest that the balance of gut bacteria will be
affected"[27] by the conversion of NAG to glufosinate.

When eating Liberty Link corn, we not only consume NAG, but also the pat and
bar genes with their pat and bar proteins. It is possible that when NAG is
converted to herbicide in our gut, the pat protein, for example, might
reconvert some of the herbicide back to NAG. This might lower concentrations
of glufosinate inside of our gut. On the other hand, some microorganisms may
be able to convert in both directions, from glufosinate to NAG and also back
again. If the pat protein can do this, that is, if it can transform NAG to
herbicide, than the presence of the pat protein inside our gut might
regenerate more herbicide from the ingested NAG. Since there are no public
studies on this, we do not know if consuming the pat gene or bar genes will
make the situation better or worse.

But one study on the pat gene raises all sorts of red flags. German
scientist Hans-Heinrich Kaatz demonstrated that the pat gene can transfer
into the DNA of gut bacteria. He found his evidence in young bees that had
been fed pollen from glufosinate-tolerant canola plants. The pat gene
transferred into the bacteria and yeast inside the bees' intestines. Kaatz
said, "This happened rarely, but it did happen."[28] Although no studies
have looked at whether pat genes end up in human gut bacteria, the only
human GM-feeding study ever conducted did show that genetic material can
transfer to our gut bacteria. This study, published in 2004, confirmed that
portions of the Roundup-tolerant gene in soybeans transferred to microor
ganisms within the human digestive tract.[29]

Since the pat gene can transfer to gut bacteria in bees, and since genetic
material from another GM crop can transfer to human gut bacteria, it is
likely that the pat gene can also transfer from Liberty Link corn or
soybeans to our intestinal flora. If so, a key question is whether the
presence of the pat gene confers some sort of survival advantage to the
bacteria. If so, "selection pressure" would favor its long term
proliferation in the gut.

Because the pat protein can protect bacteria from being killed by
glufosinate, gut bacteria that take up the gene appears to have a
significant survival advantage. Thus, the gene may spread from bacteria to
bacteria, and might stick around inside us for the long-term. With more pat
genes, more and more pat protein is created. The effects of long-term
exposure to this protein have not been evaluated.

Now suppose that the pat protein can also re-toxify NAG back into active
herbicide, as discussed above. A dangerous feedback loop may be created: We
eat Liberty Link corn or soy. Our gut bacteria, plus the pat protein, turns
NAG into herbicide. With more herbicide, more bacteria are killed. This
increases the survival advantage for bacteria that contain the pat gene. As
a consequence, more bacteria end up with the gene. Then, more pat protein is
produced, which converts more NAG into herbicide, which threatens more
bacteria, which creates more selection pressure, and so on. Since studies
have not been done to see if such a cycle is occurring, we can only
speculate.

Endocrine disruption at extremely low doses

Another potential danger from the glufosinate-tolerant crops is the
potential for endocrine disruption. Recent studies reveal that
endocrine-disrupting chemicals (EDCs) can have significant hormonal effects
at doses far below those previously thought to be significant. The
disruptive effects are often found only at minute levels, which are measured
in parts per trillion or in the low parts per billion. This is seen, for
example, in the way estrogen works in women. When the brain encounters a
mere 3 parts per trillion, it shuts down production of key hormones. When
estrogen concentration reaches 10 parts per trillion, however, there is a
hormone surge, followed by ovulation.

Unfortunately, the regulation and testing of agricultural chemicals,
including herbicides, has lagged behind these findings of extremely low dose
effects. The determination of legally acceptable levels of herbicide
residues on food was based on a linear model, where the effect of toxic
chemicals was thought to be consistent and proportional with its dosage. But
as the paper Large Effects from Small Exposures shows, this model
underestimates biological effects of EDCs by as much as 10,000 fold.[30]

In anticipation of their (not-yet-commercialized) Liberty Link rice, Bayer
CropScience successfully petitioned the EPA in 2003 to approve maximum
threshold levels of glufosinate ammonium on rice. During the comment period
preceding approval, a Sierra Club submittal stated the following.

"We find EPA's statements on the potential of glufosinate to function as an
endocrine-disrupting substance in humans and animals as not founded on
logical information or peer-reviewed studies. In fact EPA states that no
special studies have been conducted to investigate the potential of
glufosinate ammonium to induce estrogenic or other endocrine effects. . . .
We feel it's totally premature for EPA at this time to dismiss all concerns
about glufosinate as an endocrine-disrupting substance. . . . Due to the
millions of Americans and their children exposed to glufosinate and its
metabolites, EPA needs to conclusively determine if this herbicide has
endocrine-disrupting potential."

The EPA's response was that "glufosinate ammonium may be subjected to
additional screening and/or testing to better characterize effects related
to endocrine disruption" but this will only take place after these protocols
are developed. In the mean time, the agency approved glufosinate ammonium
residues on rice at 1 part per million.

Since glufosinate ammonium might have endocrine disrupting properties, even
small conversions of NAG to herbicide may carry significant health risks for
ourselves and our children.

The EPA's response was that "glufosinate ammonium may be subjected to
additional screening and/or testing to better characterize effects related
to endocrine disruption"  but this will only take place after these
protocols are developed. In the mean time, the agency approved glufosinate
ammonium residues on rice at 1 part per million.

Since glufosinate ammonium might have endocrine disrupting properties, even
small conversions of NAG to herbicide may carry significant health risks for
ourselves and our children.

Inadequate animal feeding studies

If we look to animal feeding studies to find out if Liberty Link corn
creates health effects, we encounter what independent observers have
expressed for years-frustration. Industry-sponsored safety studies, which
are rarely published and often kept secret, are often described as designed
to avoid finding problems.

If we look to animal feeding studies to find out if Liberty Link corn
creates health effects, we encounter what independent observers have
expressed for years-frustration. Industry-sponsored safety studies, which
are rarely published and often kept secret, are often described as designed
to avoid finding problems.

In a 42-day feeding study on chickens, for example, 10 chickens (7%) fed
Liberty Link corn died compared to 5 chickens eating natural corn.  Even
with the death rate doubled, "because the experimental design was so
flawed," said bio-physicist Mae-Wan Ho, "statistical analysis failed to
detect a significant difference between the two groups."  Similarly,
although the GM-fed group gained less weight, the study failed to recognize
that as significant. According to testimony by two experts in chicken
feeding studies, the Liberty Link corn study wouldn't identify something as
significant unless there had been "huge" changes. The experts said, "It may
be worth noting, in passing, that if one were seeking to show no effect, one
of the best methods to do this is would be to use insufficient replication,
a small n," which is exactly the case in the chicken study.

Without adequate tests and with a rubber stamp approval process, GM crops
like Liberty Link corn may already be creating significant hard-to-detect
health problems. In Europe, Japan, Korea, Russia, China, India, Brazil and
elsewhere, shoppers have the benefit of laws that require foods with GM
ingredients to be labeled. In the US, however, consumers wishing to avoid
them are forced to eliminate all products containing soy and corn, as well
as canola and cottonseed oils. Or they can buy products that are organic or
say "non-GMO" on the package. Changing one's diet is a hassle, but with the
hidden surprises inside GM foods, it may be a prudent option for
health-conscious people, especially young children and pregnant women.


Jeffrey Smith is the author of the international bestseller, Seeds of
Deception. The information in this article presents some of the numerous
health risks of GM foods that will be presented in his forthcoming book,
Genetic Roulette: The documented health risks of genetically engineered
foods, due out in the fall.

   _____

Spilling the Beans is a monthly column available at
www.responsibletechnology.org

Permission is granted to publishers and webmasters to reproduce issues of
Spilling the Beans in whole or in part. Just email us at
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   _____


[1] Liberty Link is a registered trademark of Bayer CropScience.

[2] http://www.pioneer.com/canada/crop_management/fsllink.htm

[3] Roundup is a registered trademark of Monsanto.

[4] Charles Benbrook, "Genetically Engineered Crops and Pesticide Use in the
United States: The First Nine Years," October 2004
http://www.biotech-info.net/Technical_Paper_6.pdf

[5] Colanduoni JA and Villafranca JJ (1986). Inhibition of Escherichia coli
glutamine-synthetase by phosphinothricin. Bioorganic Chemistry 14(2):
163-169, and Pline W A~ Lacy GH~ Stromberg V ~ Hatzios KK (200 I).
Antibacterial activity of the herbicide glufosinate on Pseudomonas syringae
pathovar glycinea. Pesticide Biochemistry And Physiology 71(1): 48-55.

[6] Liu CA; Zhong H; Vargas J; Penner D; Sticklen M (1998). Prevention of
fungal diseases in transgenic, bialaphos- and glufosinate-resistant creeping
bentgrass (Agrostis palustrls). Weed Science 46(1): 139-146, and Tada T~
Kanzaki H~ Norita E~ Uchimiya H~ Nakamura I (1998). Decreased symptoms of
rice blast disease on leaves of bar-expressing transgenic rice plants
following treatment with bialaphos. Molecular Plant-Microbe Interactions
9(8): 762-764.

[7] Ahn Y -J, Kim Y -J and Yoo J-K (2001). Toxicity of the herbicide
glufosinate-ammonium to predatory insects and mites of Tetranychus urticae
(Acari: Tetranychidae) under laboratory conditions. Journal Of Economic
Entomology 94(1): s157-161.

[8] Watanabe T and Sano T (1998). Neurological effects of glufosinate
poisoning with a brief review. Human & Experimental Toxicology 17(1): 35-39.

[9] Bremmer IN and Leist K-H (1997). Disodium-N-acetyl-L-glufosinate; AE
F099730 - Hazard evaluation of Lglufosinate produced intestinally from
N-acetyl-L-glufosinate. Hoechst Schering AgrEvo GmbH, Safety Evaluation
Frankfurt. TOX97/014. A58659. Unpublished. (see FAO publication on
www.fao.org/ag/agp/agpp/pesticid/jmpr/Download/98/glufosi3.pdf

[10] Kellner H-M, StumpfK and Braun R (1993). Hoe 099730-14C
Pharmacokinetics in rats following single oral and intravenous
administration of3 mg/kg body. Hoechst RCL, Germany, 01-L42-0670-93. A49978.
Unpublished.

[11] Huang, M.N. and Smith, S.M. 1995b. Metabolism of [14C]-N-acetyl
glufosinate in a lactating goat. AgrEvo USA Co.Pikeville, PTRL East Inc.,
USA. Project 502BK. Study U012A/A524. Report A54155. Unpublished.
http://www.fao.org/WAICENT/FAOINFO/AGRICULT/AGP/AGPP/Pesticid/JMPR/Download/
98_eva/glufosi.pdf

[12] In one study, for example, protein produced from a gene found in E.
coli turned NAG into glufosinate. G. Kriete et al, Male sterility in
transgenic tobacco plants induced by tapetum-specific deacetylation of the
externally applied non-toxic compound N-acetyl-L-phosphinothricin, Plant
Journal, 1996, Vol.9, No.6, pp.809-818.

[13] Bremmer IN and Leist K-H (1998). Disodium-N-acetyl-L-glufosinate (AE
F099730, substance technical) - Toxicity and metabolism studies summary and
evaluation. Hoechst Schering AgrEvo, Frankfurt. TOX98/027. A67420.
Unpublished. (see FAO publication on
www.fao.org/ag/agp/agpp/pesticid/jmpr/Download/98/glufosi3.pdf

[14] Huang, M.N. and Smith, S.M. 1995b. Metabolism of [14C]-N-acetyl
glufosinate in a lactating goat. AgrEvo USA Co.Pikeville, PTRL East Inc.,
USA. Project 502BK. Study U012A/A524. Report A54155. Unpublished.

http://www.fao.org/WAICENT/FAOINFO/AGRICULT/AGP/AGPP/Pesticid/JMPR/Download/
98_eva/glufosi.pdf

[15] Ricarda A. Steinbrecher, Risks associated with ingestion of Chardon LL
maize, The reversal of N-acetyl-L- glufosinate to the active herbicide
L-glufosinate in the gut of animals, Chardon LL Hearing, May 2002, London.
(Note: This work is an excellent summary of the risks associated with NAG
conversion within the gut.)

[16] Fujii, T., Transgenerational effects of maternal exposure to chemicals
on the functional development of the brain in the offspring. Cancer Causes
and Control, 1997, Vol. 8, No. 3, pp. 524-528..

[17] H. Takahashi et al., "A Case of Transient Diabetes Isipidus Associated
with Poisoning by a Herbicide Containing Glufosinate." Clinical Toxicology
38(2), 2000, pp.153-156.

[18] Ohn J. Fialka, EPA Scientists Pressured to Allow Continued Use of
Dangerous Pesticides, Wall Street Journal Page A4, May 25, 2006,
http://online.wsj.com/article/SB114852646165862757.html

[19] EPA SCIENTISTS PROTEST PENDING PESTICIDE APPROVALS; Unacceptable Risk
to Children and Political Pressure on Scientists Decried, Press release,
Public Employees for Environmental Responsibility. May 25, 2006,
http://www.peer.org/news/news_id.php?row_id=691

[20] EPA SCIENTISTS PROTEST PENDING PESTICIDE APPROVALS; Unacceptable Risk
to Children and Political Pressure on Scientists Decried, Press release,
Public Employees for Environmental Responsibility. May 25, 2006,
http://www.peer.org/news/news_id.php?row_id=691

[21] Bayer's GE Crop Herbicide, Glufosinate, Causes Brain Damage, The Japan
Times, 7 December 2004.

[22] Watanabe, T. and T. Iwase, Development and dymorphogenic effects of
glufosinate ammonium on mouse embryos in culture. Teratogenesis
carcinogenesis and mutagenesis, 1996, Vol. 16, No. 6, pp. 287-299.

[23] Watanabe, T. , Apoptosis induced by glufosinate ammonium in the
neuroepithelium of developing mouse embryos in culture. Neuroscientific
Letters, 1997, Vol. 222, No. 1, pp.17-20, as cited in Glufosinate ammonium
fact sheet, Pesticides News No.42, December 1998, p 20-21.

[24] Fujii, T., Transgenerational effects of maternal exposure to chemicals
on the functional development of the brain in the offspring. Cancer Causes
and Control, 1997, Vol. 8, No. 3, pp. 524-528.

[25] Fujii, T., T. Ohata, M. Horinaka, Alternations in the response to
kainic acid in rats exposed to glufosinate-ammonium, a herbicide, during
infantile period. Proc. Of the Japan Acad. Series B-Physical and Biological
Sciences, 1996, Vol. 72, No. 1, pp. 7-10.

[26] Bayer's GE Crop Herbicide, Glufosinate, Causes Brain Damage, The Japan
Times, 7 December 2004.

[27] Ricarda A. Steinbrecher, Risks associated with ingestion of Chardon LL
maize, The reversal of N-acetyl-L- glufosinate to the active herbicide
L-glufosinate in the gut of animals, Chardon LL Hearing, May 2002, London.
(Note: This work is an excellent summary of the risks associated with NAG
conversion within the gut.)

[28] Antony Barnett, New Research Shows Genetically Modified Genes Are
Jumping Species Barrier, London Observer, May 28, 2000.

[29] Netherwood, et al, Assessing the survival of transgenic plant DNA in
the human gastrointestinal tract, Nature Biotechnology, Vol 22 Number 2
February 2004.

[30] Wade V. Welshons et al, Large Effects from Small Exposures. I.
Mechanisms for Endocrine-Disrupting Chemicals with Estrogenic Activity,
Table 2,Environmental Health Perspectives Volume 111, Number 8, June 2003.

[31]  Glufosinate Ammonium; Pesticide Tolerance, Environmental Protection
Agency, Federal Register: September 29, 2003 (Volume 68, Number 188), 40 CFR
Part 180, ACTION: Final rule,
http://www.epa.gov/fedrgstr/EPA-PEST/2003/September/Day-29/p24565.htm

[32] S. Leeson, The effect of Glufosinate Resistant Corn on Growth of Male
Broiler Chickens, by Department of Animal and Poultry Sciences, University
of Guelph. Report No. A56379; July 12, 1996.

[33] Mae-Wan Ho, Exposed: More Shoddy Science in GM Maize Approval, ISIS
Press Release 13/03/04,  http://www.i-sis.org.uk/MSSIGMMA.php

[34] Testimony of Steve Kestin and Toby Knowles, Department of Clinical
Veterinary Science, University of Bristol on behalf of Friends of the Earth,
before the Chardon LL Hearings of the Advisory Committee on Releases to the
Environment, November 2000.

[35] Testimony of Steve Kestin and Toby Knowles, Department of Clinical
Veterinary Science, University of Bristol on behalf of Friends of the Earth,
before the Chardon LL Hearings of the Advisory Committee on Releases to the
Environment, November 2000.

   _____

C Copyright 2006 by Jeffrey M. Smith.

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