Good News About Glufosinate (Liberty) Herbicide: Most is washed off in Rain, Stays Put in Leaves, Or Flushed Down The Toilet..

Jeffrey Smith, author of the coming book Genetic Roulette, has come out with a preview of a book chapter that's appearing at several blogs.

It's all about the possible toxicity of the herbicide glufosinate (known commercially as Liberty),

This broad spectrum herbicide is marketed by Bayer in North America in association with herbicide tolerant crops such as GM hybrid canola, and Pioneer Hi-Bred's Liberty Link corn. (Other common names used for the herbicide are glyfosinate, BASTA).

Such GM crops are tolerant to glufosinate due to their ability to convert it into an inactive form that chemists call N-Acetyl-glufosinate, and which we'll call NAG for simplicity.

Jeffrey's new article starts:

Pioneer Hi-Bred's website boasts that their genetically modified (GM) Liberty Link 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." 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...

Jeffrey seems to be hinting there is some kind of cover-up of the fact that inactivated glufosinate persists in plant tissues, and another coverup of the fact that gut bacteria can convert NAG back to glufosinate in the gut.

Jeffrey is working up a big story about possible toxicity of GM crops and feeds based on this allegedly covered-up theme.

But if one is making money out of with scare stories in a book, the right thing to do is make sure the readers know which parts of the book are new, and which parts have already been factored into safety assessments by the regulators. Jeffrey doesn't do this .

Here's what's missing.

There has been no cover up about NAG. The issues bought up by Jeffrey are all openly discussed in scientific papers going back over ten years or more and in numerous submissions to regulatory agencies.

Regulatory agencies include the inactive version of NAG in their safe level assessment exactly because it could be converted to toxic glufosinate, as NAG's persistance in plants has been part of the open scientific literature and well known to regulatory agencies. Reactivation of NAG by gut bacteria is also well known.

But very little glufosinate or NAG gets in the seeds which are the part eaten by humans. Most of it goes elsewhere in the plant, and it mainly stays put in the leaves, and a lot gets washed off by rain. Negligible amounts get into oils.

A key paper that Jeffrey Smith omits is Ruhland, Engelhardt and Pawlizki, (2004) Pest Management Science 60: 691-696.

These scientists found that the residues of glufosinate at harvest mostly remained in treated leaves, and at harvest-time, levels were lowest in the grains (0.07–0.3% in maize and 0.4–0.6% in oilseed rape). They found no indication of an accumulation of total herbicide residues or of residue levels above the official tolerances for glufosinate.

Thus only very low levels of glufosinate or NAG might be present in foods, and on top of this, only a minor percentages of NAG gets converted to active glufosinate in the gut.

What's more, at low levels in food or feed, most of the NAG in the gut gets excreted in faeces. The lower the amount fed to animals, the less percentwise that gets absorbed into the body because low concentrations slow the absorbsion process.

That right, it's safely flushed down the toilet.

For example at a dose level of 3 mg/kg body weight NAG fed to a rat, 96-100% appears in its faeces after 48 hours.

Finally animals have more flexible ways of managing the effects of glufosinate than plants.

Animals have elaborate mechanism for dealing with nitrogen-metabolism and ammonia (which glufosinate affects) that plants don't have.

The FAO WHO agencies put it this way :

In plants, glutamine synthetase is the main enzyme involved in the control of ammonia concentrations, and its inhibition is the mechanism of action of glufosinate-ammonium in plants.

In mammals, other pathways exist for the homeostatic control of ammonia, such as reverse reaction of amino acid dehydrogenases and the carbamoyl phosphate synthetase-urea cycle...

The liver has two distinct systems for dealing with ammonia. A high-capacity, low-affinity system exists in the periportal hepatocytes which is based on carbamoyl phosphate synthetase and the urea cycle. In central vein hepatocytes, a low-capacity, high-affinity system exists which is based on glutamine synthetase and ornithine aminotransferase. Hack et al. (1994) showed that doses of glufosinate-ammonium did not increase ammonia concentrations in liver at a dose (5000 ppm) that inhibited glutamine synthetase activity by 50%. While a 60% reduction in liver glutamine was seen at day 1, the concentration had returned to normal by day 4, indicating the induction of alternative pathways. Inhibition of liver glutamine synthetase by up to 50% is therefore not considered to be adverse in isolation.