Glyphosate

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Glyphosate, N-phosphonomethyl glycine, is broad-spectrum herbicide, sold under the brand name Roundup classified as an organophosphorus herbicide[1] and it is "the most widely used broad-spectrum herbicide on [a] global scale."[2] Glyphosate was labelled a probable human carcinogen, hazardous to workers and consumers, by the World Health Organization in 2015. "The new classification by the International Agency for Research on Cancer, a branch of the World Health Organization, is based on research on human exposure in the U.S., Canada and Sweden and on animal studies that found what the agency called “convincing evidence” that the chemical caused cancer in laboratory animals."[3]

Commercial formulations of glyphosate were first sold in 1974.[4] Some genetically engineered crops, called Roundup Ready Crops, have their DNA altered to allow them to withstand glyphosate. These include Roundup Ready soybeans, corn, canola, sugarbeets, and alfalfa. Due to the overuse of glyphosate based herbicides, many weeds have evolved resistance to glyphosate.

History

Glyphosate's usefulness as an herbicide was discovered by Monsanto scientist John E. Franz in 1970.[5] It was first introduced in the herbicide Roundup by Monsanto in 1974.[6] Glyphosate is the active ingredient in Roundup, but the product also includes water and a surfactant, polyoxyethylene-alkylamine (POEA), which allows the herbicide to adhere to a plant's leaves so that the active ingredient can penetrate them. As of 2005, Monsanto's glyphosate products alone were registered in more than 130 countries for use in more than 100 crops.

Much of Roundup's success is due to the perception that it is safe and nontoxic, as well as the fact that it is effective against so many species of plants. However, its safety is the subject of controversy. In 2005, Monsanto wrote:

"Glyphosate binds tightly to most types of soil so it is not available for uptake by roots of nearby plants. It works by disrupting a plant enzyme involved in the production of amino acids that are essential to plant growth. The enzyme, EPSP synthase, is not present in humans or animals, contributing to the low risk to human health from the use of glyphosate according to label directions."[6]

Another description reads:

"The broad-spectrum, post-emergence, glyphosate-containing herbicide Roundup® eliminates over 125 kinds of annual and perennial weeds. It is not active in soil and is readily metabolized to innocuous products... Glyphosate inhibits a key enzyme found primarily in plants, having no effect on mammals, birds, fish, or insects. Roundup® allows farmers to control weeds with minimal tillage, conserving topsoil, time, and fuel."[7]

Roundup has won awards due to its perception of effectiveness and safety. In 1987, Franz received the National Medal of Technology for his work on glyphosate. In September 1994, Farm Chemicals magazine named Roundup one of the "Top 10 Products That Changed the Face of Agriculture." In 1996, Monsanto received the Presidential Award for Sustainable Development for "pioneering sustainable technologies" including glyphosate. The same year, Monsanto received the Presidential Green Chemistry Challenge Award for "environmentally responsible systems used in the manufacture of glyphosate herbicides.[6]

The first Roundup Ready GMO crops, soybeans, were introduced by Monsanto in 1996.[8] The same year, the first Glyphosate Resistant Weeds began to emerge.[9]

Glyphosate Products

Glyphosate is the active ingredient in a number of herbicide products including:

Most, if not all, glyphosate products contain inactive ingredients in addition to glyphosate.

How It Works

Glyphosate is absorbed through a plant's foliage and then transported throughout the stems, leaves, and roots of the entire plant.

"Glyphosate inhibits plant growth by inhibiting the production of essential aromatic amino acids through competitive inhibition of the enzyme enolpyruvylshikimate phosphate (EPSP) synthase. This is a key enzyme in the shikimic acid pathway for the synthesis of chorismate..., which is a precursor for the essential amino acids phenylalanine, tyrosine, and tryptophan."[10]

In other words, glyphosate prevents plants from making amino acids they need to survive. It does this by inhibiting an enzyme needed to make chorismate, a precursor to those amino acids. One of these amino acids, tryptophan, "is necessary for the synthesis of indolylacetic acid (IAA), the main growth promoter, that can explain the widespread field observation of reduced in depth root growth of plants."[11]

A 1984 study found plants that died following treatment with glyphosate were infected with pathogenic fungi, compared to control plants not treated with glyphosate but planted in the same media that did not yield pathogenic fungi.[12] The study concluded that more research was needed but postulated that glyphosate inhibits the plant's defense mechanisms and/or increases nutrient leakage from treated plants.

When more research was completed, "Rahe and coworkers documented that severe root infection associated with glyphosate-treated plants was due to disruption of synthesis of plant defense compounds, or phytoalexins, through the shikimate pathway there by predisposing plants to attack by soilborne fungal pathogens (Johal and Rahe, 1988; Lévesque et al., 1987).[13][14] Thus, infection by soilborne pathogens caused by the inability of plants to synthesize phytoalexins contributed to the overall herbicidal efficacy of glyphosate and was considered a “secondary mode of action” of glyphosate. These findings were significant because the release of glyphosate into the environment was found to have considerably more and far-reaching effects than the original notion that was limited to only the localized disruption of a specific metabolic pathway within a target plant."[15]

Is Glyphosate Safe?

As noted above, glyphosate has been marketed as safe since its commercialization in 1974. However, there are some questions about its safety, its inactivity in the environment, and even its herbicidal mode of action (i.e. how it kills plants).

Studies Indicate Glyphosate is Probable Human Carcinogen

Glyphosate was labelled a probable human carcinogen, hazardous to works and consumers, by the World Health Organization in 2015. "The new classification by the International Agency for Research on Cancer, a branch of the World Health Organization, is based on research on human exposure in the U.S., Canada and Sweden and on animal studies that found what the agency called “convincing evidence” that the chemical caused cancer in laboratory animals."[16]


Impact on Animals and Humans

A 2010 study found that low doses of glyphosate cause birth defects in frogs and chickens. The study was undertaken due to "reports of neural defects and craniofacial malformations from regions where [glyphosate based herbicides] are used heavily."[17] The study cited previous research on glyphosate based herbicides, noting:

  • Two 2002 studies found that surfactants in glyphosate formations facilitate penetration of glyphosate through cell membranes.[18][19]
  • A 2005 study found that a glyphosate based herbicide act as an endocrine disruptor in a culture of placental cells.[20] ("GBH acts as an endocrine disruptor in cultures of JEG3 placental cells, decreasing the mRNA levels of the enzyme CYP19 (an essential component of cytochrome p450 aromatase) and inhibiting its activity. CYP19 is responsible for the irreversible conversion of androgens into estrogens. The GBH Roundup is able to disrupt aromatase activity. Importantly, the active principle glyphosate interacts with the active site of the purified enzyme and its effects in cell cultures, and microsomes are facilitated by other components in the Roundup formulation that presumably increase the bioavailability of glyphosate."[21])
  • Two 2009 studies found that glyphosate and its commercial formulations "severely affect embryonic and placental cells, producing mitochondrial damage, necrosis, and programmed cell death by the activation of caspases 3/7 in cell culture within 24 h with doses far below those used in agriculture. Other effects observed include cytotoxicity and genotoxicity, endocrine disruption of the androgen and estrogen receptors, and DNA damage in cell lines."[21][22][23]
  • A study published in 2012 found that Roundup in formulation -- including glyphosate and inactive ingredients like adjuvants that help the product penetrate cells -- caused mammary and kidney tumors in rats, who were given water spiked with Roundup over their entire 600-day lifespan.[24] For more, see "Study Links NK603 to Tumors in Rats."

A 2011 report, which examines industry studies and regulatory reports, claiming to show that "industry and regulators knew as long ago as the 1980s and 1990s that glyphosate causes malformations - but that this information was not made public." It says:[25]

"Scientific research published in 2010 showed that Roundup and the chemical on which it is based, glyphosate, cause birth defects in frog and chicken embryos at dilutions much lower than those used in agricultural and garden spraying. The EU Commission dismissed these findings, based on a rebuttal provided by the German Federal Office for Consumer Protection and Food Safety, BVL. BVL cited unpublished industry studies to back its claim that glyphosate was safe.
"The Commission has previously ignored or dismissed many other findings from the independent scientific literature showing that Roundup and glyphosate cause endocrine disruption, damage to DNA, reproductive, and developmental toxicity, neurotoxicity, and cancer, as well as birth defects. Many of these effects are found at very low doses, comparable to levels of pesticide residues found in food and the environment."

It continues, claiming that:

  • "Industry (including Monsanto) has known since the 1980s that glyphosate causes malformations in experimental animals at high doses
  • "Industry has known since 1993 that these effects could occur at lower and mid doses
  • "The German government has known since at least 1998 that glyphosate causes malformations
  • "The EU Commission's expert scientific review panel knew in 1999 that glyphosate causes malformations
  • "The EU Commission has known since 2002 that glyphosate causes malformations."

Monsanto responded, calling the scientists' claims false[26] and the scientists responded to Monsanto, standing by their accusations.[27]

Impact on Non-Target Plants

Once glyphosate travels to a plant's roots, it is "released into the rhizosphere," (the area immediately around the roots), "where it is immobilized at the soil matrix or microbially degraded.[28] However, some of the glyphosate remains in dead plant tissues. A 2009 study found that non-target plants continue to be impacted by glyphosate toxicity up to three weeks after glyphosate application.[29]

A 2009 study examined the relationship between previous glyphosate use, tillage method (conventional, minimal, or no-till), and plant diseases caused by fungal pathogens of the genus Fusarium.[30] The study found "a relationship between previous glyphosate use and increased Fusarium infection of spikes and subcrown internodes of wheat and barley, or Fusarium colonization of crop residues." However, the study adds, "because of the close association between noncereal crops, reduced tillage, and glyphosate use, it was not possible to completely separate the effects of these factors on Fusarium infections." (No-till or minimum till practices are often combined with herbicide use, specifically, glyphosate use. Thus, the scientists were not able to determine whether any increase or decrease in plant disease was related to tillage strategy, glyphosate use, or both.) The study recommended more research in this area.

Impacts of Glyphosate Drift

At sub-lethal doses of glyphosate, such as the amounts a plant might be exposed to from spray drift, plants are still impacted. A study examined sunflowers treated with small amounts of glyphosate (to simulate spray drift) found:[31]

"In conclusion, the results presented in this study showing that glyphosate is especially inhibitory to ferric reductase complement the recently published report (Eker etal., 2006) that glyphosate exerts a strong inhibitory influence on ferric reductase activity of Fe-deficient roots and impairs the uptake and translocation of Fe in plants. These impairments could be a major reason for the increasingly observed Fe deficiency chlorosis in cropping systems associated with widespread glyphosate usage as reported for different parts of the USA (Franzen etal., 2003; Jolley etal., 2004). Such strong interference of glyphosate with root uptake and root-to-shoot transport of Fe in crop plants may represent a potential threat to human and animal nutrition because of possible reduction of Fe in edible plants parts (e.g. seed/grain)."

In other words, low doses of glyphosate equal to the amount plants are exposed to in spray drift, can result in iron deficiencies in the plants. For crops destined as animal feed or as human food, this could result in decreased dietary iron.

Impact on Microorganisms

Several sources have found that glyphosate impacts soil microorganisms. For example:

"Subsequent research on glyphosate interactions with soil microorganisms demonstrated that although glyphosate was metabolized by a segment of the microbial population, it was also toxic to several bacteria and fungi; the net effect glyphosate appeared to be a disruption of soil and root microbial community composition because selected components of the microbial community were stimulated while others were suppressed."[32][33][34]
"Herbicides, including glyphosate, can inhibit or stimulate the growth of fungal pathogens, and can either increase or decrease disease development through direct or indirect means (Altman, 1993; Levesque and Rahe, 1992).[35][36] Levesque and Rahe (1992) showed evidence that herbicides can have a direct effect on various components of the soil microflora, such as plant pathogens, antagonists, or mycorrhizae, which can potentially increase or decrease the incidence of plant disease. Pathogens able to infect weeds can also increase their inoculum potential after weeds have been sprayed with herbicides, which could subsequently affect host crops."[37]

Glyphosate in the Environment

Although glyphosate is highly soluble in water, its tendency to bond to soils makes it unlikely to leach into groundwater or runoff "significantly." (Studies have found about 1%-2% of glyphosate may runoff in rainfall after glyphosate is applied.[38])

Glyphosate in the Soil

Glyphosate can reach the soil by washing off the foliage of plants, via spray drift, by exudation from the roots of treated plants, or by the decomposition of treated plants. However, "risks of glyphosate toxicity to non-target organisms in soils are generally considered as marginal,since glyphosate is almost instantaneously inactivated by adsorption to clay minerals and cationic binding sites of the soil matrix (Piccoloetal.,1992;Dong-Meietal.,2004), while glyphosate in the soil solution is prone to rapid microbial degradation (Giesy et al., 2000)."[39][40] In other words, glyphosate residues in the soil are not considered hazardous as it either breaks down quickly or binds to minerals that make it no longer a threat to plants. Glyphosate that biodegrades usually breaks down into carbon dioxide and ammonium (NH4+).[41] In an analysis of 47 studies, 50% of glyphosate broke down in the soil in time periods ranging from 1.2 days to 197.3 days. The arithmetic mean amount of time was 32 days and the geometric mean was 17 days.[42]

Although glyphosate is mostly broken down by microbes or bound to the soil, a 2009 study found that "the root tissue of glyphosate-treated weeds represents a storage pool for glyphosate."[43]

Glyphosate in Water

Although most glyphosate applied to soil does not run off into waterways, sometimes glyphosate is applied to aquatic environments directly. In flowing water, it is dissipated via "tributary dilution, dispersion, and loss through processes such as absorption to suspended particulate matter or sediments and microbial degradation."[44] The half-life of glyphosate in water has been estimated to be from 7 to 14 days.[45]

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References

  1. ↑ Classification of Herbicides, Accessed August 9, 2012.
  2. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  3. ↑ Environmental Working Group, Press Release, [World Health Organization Labels Glyphosate Probable Carcinogen http://www.ewg.org/release/world-health-organization-labels-glyphosate-probable-carcinogen], March 20, 2015.
  4. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  5. ↑ Inventor of the Week: Roundup, Accessed July 12, 2012.
  6. ↑ 6.0 6.1 6.2 History of Monsanto's Glyphosate Herbicides, Monsanto, 2005.
  7. ↑ Inventor Hall of Fame: Roundup, Accessed July 12, 2012.
  8. ↑ Highlights Through the Years, Monsanto, Accessed July 14, 2012.
  9. ↑ Vijay K. Nandula, Krishna N. Reddy, Stephen O. Duke, and Daniel H. Poston, "Glyphosate-Resistant Weeds: Current Status and Future Outlook," USDA ARS.
  10. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  11. ↑ Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.
  12. ↑ Gurmukh S. Johal and James E. Rahe, "Effect of soilborne plant-pathogenic fungi on the herbicidal action of glyphosate on bean seedlings," Phytopathology (1984), 74:950-955.
  13. ↑ Johal, G.S., Rahe, J.E., 1988. Glyphosate, hypersensitivity and phytoalexins accumulation in the incompatible bean anthracnose host-parasite interaction. Physiol. Mol. Plant Pathol. 32, 267-281
  14. ↑ Lévesque, C.A., Rahe, J.E., Eaves, D.M., 1987. Effects of glyphosate on Fusarium spp.: its influence on root colonization of weeds, propagule density in the soil, and crop emergence. Can. J. Microbiol. 33, 354-360.
  15. ↑ Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.
  16. ↑ Environmental Working Group, Press Release, [World Health Organization Labels Glyphosate Probable Carcinogen http://www.ewg.org/release/world-health-organization-labels-glyphosate-probable-carcinogen], March 20, 2015.
  17. ↑ Paganelli, A., Gnazzo, V. et al. 2010. Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling. Chem Res Toxicol 23(10): 1586–1595.
  18. ↑ Haefs, R., Schmitz-Eiberger, M., Mainx, H. G., Mittelstaedt, W., and Noga, G. (2002) Studies on a new group of biodegradable surfactants for glyphosate. Pest. Manag. Sci. 58, 825–833.
  19. ↑ Marc, J., Mulner-Lorillon, O., Boulben, S., Hureau, D., Durand, G., and Belle, R. (2002) Pesticide Roundup provokes cell division dysfunction at the level of CDK1/cyclin B activation. Chem. Res. Toxicol. 15, 326–331.
  20. ↑ Richard, S., Moslemi, S., Sipahutar, H., Benachour, N., and Seralini, G. E. (2005) Differential effects of glyphosate and roundup on human placental cells and aromatase. EnViron Health Perspect 113, 716– 720.
  21. ↑ 21.0 21.1 Paganelli, A., Gnazzo, V. et al. 2010. Glyphosate-based herbicides produce teratogenic effects on vertebrates by impairing retinoic acid signaling. Chem Res Toxicol 23(10): 1586–1595.
  22. ↑ Benachour, N., and Seralini, G. E. (2009) Glyphosate formulations induce apoptosis and necrosis in human umbilical, embryonic, and placental cells. Chem. Res. Toxicol. 22, 97–105.
  23. ↑ Gasnier, C., Dumont, C., Benachour, N., Clair, E., Chagnon, M. C., and Seralini, G. E. (2009) Glyphosate-based herbicides are toxic and endocrine disruptors in human cell lines. Toxicology 262, 184–191.
  24. ↑ Gilles-Eric Séralini, Emilie Clair, Robin Mesnage, Steeve Gress, Nicolas Defarge, Manuela Malatesta, Didier Hennequin, Joël Spiroux de Vendômois, "Long term toxicity of a Roundup herbicide and a Roundup-tolerant genetically modified maize," Food and Chemical Toxicology, Available online September 19, 2012.
  25. ↑ Michael Antoniou, Mohamed Ezz El-Din Mostafa Habib, C. Vyvyan Howard, Richard C. Jennings, Carlo Leifert, Rubens Onofre Nodari, Claire Robinson, and John Fagan, "Roundup and Birth Defects: Is the Public Being Kept in the Dark?," Earth Open Source, June 2011.
  26. ↑ Monsanto’s Response to - Roundup and birth defects: Is the public being kept in the dark?, Monsanto, June 2011, accessed July 12, 2012.
  27. ↑ EOS Response to Monsanto - Roundup and birth defects: Is the public being kept in the dark?, Accessed July 12, 2012.
  28. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  29. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role o If waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  30. ↑ M.R. Fernandez, R.P. Zentner, P. Basnyat, D. Gehl, F. Selles, and Don Huber, "Glyphosate associations with cereal diseases caused by Fusarium spp. in the Canadian Prairies," European Journal of Agronomy (2009), 31:133-143.
  31. ↑ Levent Ozturk, Atilla Yazici, Selim Eker, Ozgur Gokmen, Volker Römheld, and Ismail Cakmak, "Glyphosate inhibition of ferric reductase activity in iron deficient sunflower roots," New Phytologist (2008), 177:899-906.
  32. ↑ Preface "Glyphosate interactions with physiology, nutrition, and diseases of plants: Threat to agricultural sustainability?", European Journal of Agronomy 31 (2009) 111-113.
  33. ↑ Wardle, D.A., Parkinson, D.A., 1992. Influence of the herbicides 2,4-D and glyphosate on soil microbial biomass and activity: a field experiment. Soil Biol. Biochem. 24, 185-186.
  34. ↑ Busse, M.D., Ratcliffe, A.W., Shestak, C.J., Powers, R.F., 2001. Glyphosate toxicity and the effects of long-term vegetation control on soil microbial community. Soil Biol. Biochem. 33, 1777-1789.
  35. ↑ Altman, J., 1993. Pesticide-pathogen interactions in plant disease. In: Altman, J.(Ed.), Pesticide Interactions in Crop Production, Beneficial and Deleterious Effects. CRC Press, Inc., Boca Raton, FL, pp. 315–332.
  36. ↑ C. André Lévesque and James E. Rahe, Herbicide Interactions with Fungal Root Pathogens, with Special Reference to Glyphosate, Annual Review of Phytopathology (1992), Vol. 30: 579-602.
  37. ↑ M.R. Fernandez, R.P. Zentner, P. Basnyat, D. Gehl, F. Selles, and Don Huber, "Glyphosate associations with cereal diseases caused by Fusarium spp. in the Canadian Prairies," European Journal of Agronomy (2009), 31:133-143.
  38. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  39. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  40. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  41. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  42. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  43. ↑ Tsehaye Tesfamariam, S. Bott, I. Cakmak, V. Römheld, G. Neumann, "Glyphosate in the rhizosphere – role of waiting times and different glyphosate binding forms in soils for phytoxicity to non-target plants," European Journal of Agronomy (2009), 31:126-132.
  44. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.
  45. ↑ John P. Giesy, Stuard Dobson, and Keith R. Solomon, 2000, "Ecotoxicological Risk Assessment for Roundup Herbicide," Rev Environ Contam Toxicol 167:35-120.

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