NTN ENVIRONMENTAL HEALTH DATA SEARCH

CHEMICAL NAME: GLYPHOSATE Isopropylamine salt of N-(phosphonomethyl) glycine

USAGE: A Schedule 5 herbicide in the form of the mono(isopropyl ammonium) salt. A broad spectrum (non selective) post-emergent plant growth regulator used for the control of grasses, sedges and broadleaved weeds.

A systemic herbicide that translocates to the roots of plants. Used as the active constituent in many commercial herbicide products. Formerly a Monsanto-held patent, glyphosate products are now formulated by a number of pesticide producers. Used in forestry, farming and pastoral activities, local councils, weed control and transport agencies, as well as domestic and industrial uses.

Lethal oral doses produce severe stress, breathing difficulties, blood in the lungs, convulsions and death.

Can cause slight skin irritation, severe eye irritation. Dust may cause mild to moderate irritation of nose and throat.

Toxicity of glyphosate formulations may be due to presence of surfactants and other additives/contaminants.

No chronic effects from human exposure reported in peer reviewed literature. ^[1]

Mouse feeding studies noted non-neoplastic changes including necrosis of hepatocytes male mice and hypertrophy in female mice.^[2] (Non-cancerous liver damage) potential for adverse human health impacts of glyphosate formulations requires more investigation.

Glyphosate is readily nitrosated to N-nitrosoglyphosate. Whilst this compound has not been assessed for carcinogenicity potential, at least 3/4 of another 120 N-nitroso compounds showed carcinogenic potential. Nitrosation occurs in the stomach by reaction of nitrite in human saliva. Standard carcinogenic tests using rats would not detect this effect since rats do not secrete nitrite in their saliva.^[4]

In 1986, the oncogenic potential of glyphosate was not fully understood. A review of a mouse cancer study noted a slight increase in renal tubular adenomas and a one- year feeding study in dogs observed a reduction of weight of pituitary gland in mid to high doses. The United States Environment Protection Agency reveiwed thses studies and concluded that the mice feeding study did not represent a safety concern because such high doses of glyphosate had been administered to the test animals. (up to 3% of total diet). They did require an additional rat study conducted at high dose levels.

In 1991, following review of the new rat study, the US EPA placed glyphosate in Group E. Evidence of non-carcinogenciity for humans.^[5]

Animal studies did not produce any effects. Diets of up to 30 mg/day did not produce any reproductive effects in male or female rats, over three generations. No teratogenic effects were observed in rabbits given up to 350 mg/kg/day on days 6-27 of pregnancy. Toxic effects noted at the highest dose in both treated animals and their offspring. ^[6]

Not mutagenic in a standardised series of tests using bacteria, cultured mammalian cells and whole animals.^[7] One study showed very weak mutagenic activity in an in vitro mammalian cell test. ^[8]

Glyphosate, or some additive to commercial glyphosate products, may cause damage to DNA via sister chromatid exchange. ^[9]

Glyphosate can affect the capacity of cells to produce energy. This occurs due to disruption of cell membrane structure. ^[10]

Further investigation of potential for cell and sub-cellular impacts is required

All commercial pesticide products are mixtures of chemical compounds. They contain the active constituent/s (a.i.) and other compounds such as solvents, surfactants, lubricants, preservatives, solubilizers and suspending agents. They may also contain impurities and/or contaminants. Some commercial glyphosate products contain the solvent POEA, which is contaminated with the carcinogen 1,4-dioxane, a common solvent used in laboratories and contained in many consumer products. According to the manufacturer, the levels of this contaminant are kept below 1 part per million ( ppm). Another contaminant is N-Nitrosoglyphosate. According to the manufacturer, levels of this contaminant are kept below 0.1 ppm.

No information is available on the human toxicity of pesticide mixtures containing glyphosate. It is often mixed with other pesticides. ^[11]

The US EPA regards glyphosate as being slightly toxic to birds, aquatic vertebrates and fish and moderately toxic to embryo and larvae.

Chronic toxicity to freshwater fish: Fathead minnow with maximum threshold concentration (MATC). >25.7 mg/L.

The use of glyphosate for vegetation control and the resulting decreased habitat complexity caused a decrease in invertebrate populations and songbird numbers (especially insectivores). One US study found the total abundance of songbirds was 36% lower on clear-cut treated with herbicides for at least three years. The effect related to the complexity of vegetation.^[12]

Toxicity to wildlife has mainly focussed on its acute toxicity to frogs. The Final Report, Acute toxicity of a herbicide to selected frog species^[13] investigated the toxicity of technical grade glyphosate and the glyphosate-based herbicide, Roundup 360. The method used was through acute bioassays with frog species common to the south-west of Western Australia. The report found that:

technical grade glyphosate and Roundup 360 can be acutely toxic to adult frogs and tadpoles in laboratory bioassays tadpoles were many times more sensitive to the herbicide formulation tested than adult frogs tadpoles were approximately an order of magnitude more sensitive to the formulation than to technical grade glyphosate the above results and the results of other studies reported in the literature tend to suggest that the surfactant used in the formulation is more harmful to aquatic animals than the glyphosate The report also stated that:

the acute toxicity value ( 48 hour LC50 or Lethal Concentration) to the juvenile Crinia insignifera was 51.8 mg/L for Roundup 360 (the commercial formulation containing the solvent) the acute toxicity value ( 48 hour LC50 or Lethal Concentration) to the juvenile Crinia insignifera was 83.6 mg/L for glyphosate alone the toxicity of Roundup to fish changes significantly with temperature and pH, with greatest toxicity at high temperature and pH. A potential hazard exists for frogs and tadpoles in shallow water bodies. Further study is required to determine the actual concentrations and persistence of the formulation in aquatic environments As a result of this study, commercial herbicide products containing the herbicide glyphosate have been reformulated, with the toxic surfactant replaced by another compound/s.

Limitations of the study : Replicating real world conditions in a laboratory is impossible and as a result, laboratory studies can only provide a guide to toxicity potential, not a definitive prediction. Professor Tyler of the University of Adelaide (Zoology) noted: ^[14]

The WA toxicity trial involved placing the animals in an exposure chamber where there would be some skin contact with the solution. However, under normal application in the environment, the application method (of boom spraying) may result in atomised spray, which may increase overall exposure potential for the animals.

All bioassays were conducted at 20 +/- 2 degrees C under ambient laboratory light. Temperatures in real world conditions may be as high as 42 degrees C (in the Northern Territory) and certainly well above 30 degrees C in northern NSW summer months.

The WA study looked at three frog species, with the bulk of the investigation focussed on two species, Crinia insignifera and Litoria moorei. Under real world conditions, many thousands of species of amphibians, invertebrates and other aquatic creatures may be exposed to herbicides and risks to the viability of their communities is not well understood. The studies have not been done.

Australia’s biodiversity is well documented and to assert negligible risk to the environment based on a small laboratory study on two localised frog species is not scientifically defensible.

The WA study investigated acute poisoning potential only. No attempt was made to investigate sub-lethal, chronic, reproductive, endocrinal or immunological effects, which may also pose significant risks to the viability of aquatic communities.

The WA study did indicate a 48 hour LC50 of 83.6 mg/L for glyphosate alone for Crinia insignifera. This is a significant level if reproduced by normal applications in the environment. Thus it is not just the formulation that may pose unacceptable risks to wildlife. The data generated by the WA study indicates both commercial formulation and the active constituent alone pose risks.

Australian research ^[15] reports that fescue and perennial ryegrass cultivars, soybean and convolvulus arvenis L. Lines displayed varying degrees of resistance to glyphosate. Genetic engineering of crops such as soy now allows this and other commercially important food crops to be sprayed with glyphosate, thus extending the potential global market for glyphosate-based products.

Slowly absorbed through the digestive system and rapidly eliminated.^[16] A urine test for glyphosate in urine is available.

Does not bio-accumulate in animal tissue but residues can be detected after exposure. Glyphosate and its metabolite, aminomethylphosphonic acid (AMPA) have been identified in the tissues, urine and faeces of rats and rabbits, in the liver in poultry, pigs and cattle and the kidney of pigs and cattle.^[17] Has been detected in rice. ^[18]

The persistence of glyphosate in the environment is variable. It is strongly bound to clay particles and is considered moderately persistent in soil. Degradation via microbial action is moderately slow. Half lives range from a few days to several months or years. The more sand in the soil, the slower the inactivation via the bounding to clay.

Application of glyphosate to sandy loam resulted in weakening of subclover planted 120 days after application. A significant decrease in nodule numbers and root weights of the plants was observed. This indicated that breakdown of glyphosate in soils with a high sand content is slow. Study recommended care in advocating glyphosate use in soils with high (>80%) sand content. ^[19]

Nitrosation: N-nitrosoglyphosate was generated in soils treated with sodium nitrate (20 ppm) and glyphosate (740 ppm) at elevated levels. The highest level generated was noted in soil of low organic matter and clay content. The formation of N-nitrosoglyphosate was not observed in soils treated with lower levels, nitrite nitrogen (2ppm) and glyphosate (5ppm).^[20]

The manufacturer claims that the product is completely biodegradable, breaking down into natural products in both soil and water. Stated half-life of 60 days in the soil, a time frame described as rapid by manufacturer. Other information indicates that breakdown time is extremely variable from a half-life of 24 days in forest soils in Ontario to 249 days in Finland.^[21]

Very little leaching capacity. Low potential to contaminate ground water as it is tightly bound to soil

Resistance has been genetically engineered into food crops such as soya beans so that this core food crop can be sprayed with glyphosate without killing it. This means that up to 200 times more glyphosate residue may be present in soy-based foods.

In the USA, Monsanto has agreed to change its advertisements for glyphosate-based products. As part of the agreement, Monsanto will discontinue the use of the terms “biodegradable” and “environmentally friendly “ in all advertising in New York State.

[1]. Canadian Centre of Occupational Health Database, CCINFO 1991. Glyphosate, 1,4-Dioxane

[3].US EPA. Health Advisory, Glyphosate. Office of Drinking Water. August 1988.

[4]. Shearer R. Consultant in genetic toxicology. Health effects of glyphosate. 1984.

[5]. 1) Pers. Com. Mick Tydens, Monsanto. 2) Monsanto Backgrounder Roundup Herbicide by Monsanto 3) Reregistration Eligibility Document for Glyphosate, (EPA 738-R-93-014). United States Environment Protection Agency, Washington, September 1993.

[9]. Vifusson @ Vyse. The effect of pesticides Dexon, captan and Roundup on sister chromatid exchange in human lymphocytes in vitro in Mutation Research (1980) 79, pp59-72.

[10]. For discussion of the biological mechanism (uncoupling of mitochondrial oxidative phosphorylation) see Clorunsungo, Bababunmi and Basair , 1979. Effect of glyphosate on rat liver mitochondria in vivo in Bull. Env. Contam. Toxicol. 22. pp. 357-364. This study does not meet US EPA requirements for toxicity assessment since the herbicide was given by injection, which is considered an inappropriate exposure route for humans. See also Pollak, J.K. The Toxicity of Chemical Mixtures; An Introduction to Recent Developments in Toxicology. CHAST, The University of Sydney 1993.

[11].Quite apart from their own toxicity, the additives that are contained in many pesticide products may cause metabolic reactions and in this way significantly enhance the toxicity of the formulation.

For example, when four organochlorine pesticides, dieldrin, endosulfan, toxaphene and chlordane were tested individually they were found to be weakly estrogenic. When two of these pesticides applied in combination, their activity increased between 160 and 1600 fold. Science 7/6/96.

[12]Roundup Information Summary. Soil and Health Association of New Zealand Inc. September 1993.

[13].Department of Environment Protection, Perth, Western Australia. Technical Series 79. June 1995.

[15].Powles S. B. And Holtum J.A.M. (Eds) Herbicide Resistance in Plants: Biology and Biochemistry. Lewis Publishers, Boca Raton. 1994. Pp. 231-235.

[18].Short, K. Quick Poison, Slow Poison. Pesticide Risk in the Lucky Country Envirobook, Sydney. 1994. p.69.

[19]. Eberbach P.L. and Douglas L.A. Persistence of Glyphosate in Sandy Loam. School of Agriculture and Forestry, The University of Melbourne 1983.

[20]. Khan and Young. N-nitrosamine formation in soil from the herbicide glyphosate. Agric. Food Chem. Vol. 25, no.6. 1977.