Synopsis of testimony to be presented at the Hague Tribunal. Professor Emeritus Don M. Huber Ph-D
Forty+ years ago, U.S. agriculture started a conversion to a primarily monochemical herbicide program focused around glyphosate (Roundup®). The near simultaneous shift from conventional tillage to no-till or minimum tillage stimulated this chemical conversion that was reinforced by the subsequent introduction of genetically modified crops tolerant to glyphosate. The introduction of genetically modified (Roundup Ready®, RR) crops has greatly increased the volume and scope of glyphosate usage, and the conversion of major segments of crop production to a monochemical herbicide strategy. The promotion of glyphosate based herbicides (GBH) as readily biodegradable, non-toxic and environmentally friendly by the Monsanto Company (masked the fact that glyphosate is a powerful mineral chelater, artificial amino acid, and broad spectrum antibiotic that interferes with mineral nutrition to increase plant, environmental, animal and human disease. Fraudulent safety reports of non-toxicity provided a false-sense of safety as adoption expanded throughout the environment (Wikipedia, 2015). Although previously over-looked, long-term damage to the soil, environment, crop, animal and human diseases have become more prevalent each year as glyphosate accumulation and residual effects escalate and become more apparent.
The extensive use of glyphosate, and the rapid adoption of genetically modified glyphosate tolerant crops such as soybean, corn, cotton, canola, sugar beets, potato and alfalfa; each with its own unknown toxicity, have greatly increased the indiscriminate application of glyphosate and intensified deficiencies of numerous essential micronutrients and some macronutrients. Additive nutrient inefficiency of the Roundup Ready® (RR) genetics and glyphosate herbicide necessitate extensive nutrient remediation, and increase the need well above previously established soil and tissue levels for nutrients considered sufficient for specific crop production. Previous sufficient nutrient levels also may be inadequate indicators in the less nutrient efficient glyphosate weed management program because of its extensive antibiotic effects on soil biology essential for nutrient cycling, soil structure, and symbiotic nutrition (Huber, 2010). Understanding glyphosate’s mode of action and impact of the RR genetics, are necessary to
understand the numerous long-term negative impacts of this monochemical system on plant nutrition and its predisposition to disease. An absolute consideration in this regard should be a much more regulated use of glyphosate, if not a total ban. Because of its persistence and broad impact on the physical-chemical and biological environment, glyphosate damage is often subtle and attributed to other causes such as drought, cool soils, deep seeding, high temperatures, crop residues, water fluctuations, etc. Some of the common symptoms of drift and residual glyphosate damage to crops presented in Table 1 reflect nutrient and disease interactions affected by glyphosate and the RR genetics as presented in scientific publications (Johal and Huber, 2009).
Understanding Glyphosate Glyphosate (N-(phosphomonomethyl)glycine) as a strong mineral chelator was first patented by Stauffer Chemical Co. in 1964 (U.S. Patent No. 3,160,632) and used to descale boilers and steam pipes.
Glyphosate chelates and immobilizes essential mineral nutrients that are essential for plant and animal physiological processes. It was subsequently patented as an herbicide and later as a general biocide whereby it immobilizes mineral co-factors (Co, Cu, Fe, Mn, Ni, Zn, etc.) essential for enzyme activity
and cell function. In contrast to some compounds that chelate with a single or only a few mineral species, glyphosate is a broad-spectrum chelator with both macro and micronutrients (Ca, Co, Cu, Fe, Mg, Mn, Ni, Zn). It is this strong, broad-spectrum chelating ability that also makes glyphosate a broadspectrum
herbicide, a potent antimicrobial agent and potent environmental toxicant since the function of numerous essential enzymes is affected (Ganson and Jensen, 1988). Primary emphasis in understanding glyphosate’s herbicidal activity has focused on inhibition of the enzyme 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) at the start of the Shikimate physiological pathway for secondary metabolism. This enzyme requires reduced FMN as a co-factor
(catalyst) whose reduction requires manganese (Mn). Thus, by immobilizing Mn by chelation, glyphosate denies the availability of reduced FMN for the EPSPS enzyme. It also can affect up to 25 other plant enzymes that require Mn as a co-factor and 290 other enzymes in both primary and secondary metabolism that require other mineral co-factors (Ca, Co, Cu, Fe, Mg, Ni, Zn). Several of these enzymes also function with Mn in the Shikimate pathway that is responsible for plant responses to stress and defense against pathogens (amino acids, hormones, lignin, phytoalexins, flavenoids, phenols, etc.). By inhibiting these enzymes, a plant becomes highly susceptible to various ubiquitous soilborne
pathogens (Fusarium, Pythium, Phytophthora, Rhizoctonia, etc.). It is this pathogenic activity that actually kills the plant as “the herbicidal mode of action” (Johal and Rahe, 1984; Levesque and Rahe, 1992, Johal and Huber, 2009). If glyphosate is not translocated to the roots because of stem boring insects or disruption of the vascular system, aerial parts of the plant may be stunted, but the plant is not killed.
Recognizing that glyphosate is a strong chelator to immobilize essential plant micronutrients provides an understanding for the various non-herbicidal and herbicidal effects of glyphosate. Glyphosate is a phloem-mobile, systemic chemical in plants that accumulates in meristematic tissues (root, shoot tip, reproductive organs, legume nodules) and is released into the rhizosphere through root exudation (from RR as well as non-RR plants) or mineralization of treated plant residues. Degradation of glyphosate in most soils is slow or non-existent since it is not readily ‘biodegradable’ and is primarily by microbial co-metabolism when it does occur. Although glyphosate can be immobilized in
soil (also spray tank mixtures, and plants) through chelation with various cat-ions (Ca, Mg, Cu, Fe, Mn, Ni, Zn), it is not readily degraded and can accumulate for years (in both soils and perennial plants).
Very limited degradation may be a “safety” feature with glyphosate since most degradation products are toxic to normal as well as RR plants. Phosphorus fertilizers can desorb accumulated glyphosate that is immobilized in soil to damage and reduce the physiological efficiency of subsequent crops .
Some of the observed affects of glyphosate are presented in table 1.
TABLE 1. Some things we know about glyphosate that influence plant nutrition and disease.
1. Glyphosate is a strong mineral chelator (for Ca, Co, Cu, Fe, Mn, Mg, Ni, Zn) – in the spray tank, in soil and in plants.
2. It is rapidly absorbed by roots, stems, and leaves, and moves systemically throughout the plant (normal and RR).
3. Accumulates in meristematic tissues (root, shoot, legume nodules, and reproductive sites) of normal and RR plants.
4. Inhibits EPSPS in the Shikimate metabolic pathway and many other plant essential enzymes.
5. Increases susceptibility to drought and disease.
6. Non-specific herbicidal activity (broad-spectrum weed control).
7. Some of the applied glyphosate is exuded from roots into soil.
8. Immobilized in soil by chelating with soil cat-ions (Ca, Co, Cu, Fe, Mg, Mn, Ni, Zn).
9. Persists and accumulates in soil and plants for extended periods (years) – it is not readily ‘biodegradable,’ but is immobilized by chelation generally.
10. Desorbed from soil particles by phosphorus and is available for root uptake by all plants.
11. Toxic to soil organisms that facilitate nutrient access, availability, or absorption of nutrients.
12. Inhibits the uptake and translocation of Fe, Mn, and Zn at very low, non-herbicidal rates.
13. Stimulates soilborne pathogenic and other soil microbes to reduce nutrient availability.
14. Reduces secondary cell wall formation and lignin in RR and non-RR plants.
15. Inhibits nitrogen fixation by chelating Ni for ureide synthesis and is toxic to Rhizobiaceae.
16. Reduces physiological availability and concentration of Ca, Cu, Fe, K, Mg, Mn, and Zn in plant tissues and seed.
17. Residual soil activity can damage plants through root uptake at 1/40th of herbicidal concentrations.
18. Increases mycotoxins in stems, straw, grain, and fruit.
19. Reduces photosynthesis (CO2 fixation).
20. Causes fruit (bud) drop and other hormonal effects.
21. Accumulates in food and feed products to enter the food chain as a concern for food safety.
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