Glyphosate and aminomethylphosphonic acid chronic risk assessment for soil biota.

Glyphosate is a broad-spectrum herbicide used widely in agriculture, horticulture, private gardens, and public infrastructure, where it is applied to areas such as roadsides, railway tracks, and parks to control the growth of weeds. The exposure risk from glyphosate and the primary soil metabolite aminomethylphosphonic acid (AMPA) on representative species of earthworms, springtails, and predatory soil mites and the effects on nitrogen-transformation processes by soil microorganisms were assessed under laboratory conditions based on internationally recognized guidelines. For earthworms, the reproductive no-observed-effect concentration (NOEC) was 472.8 mg glyphosate acid equivalent (a.e.)/kg dry soil, which was the highest concentration tested, and 198.1 mg/kg dry soil for AMPA. For predatory mites, the reproductive NOEC was 472.8 mg a.e./kg dry soil for glyphosate and 320 mg/kg dry soil for AMPA, the highest concentrations tested. For springtails, the reproductive NOEC was 472.8 mg a.e./kg dry soil for glyphosate and 315 mg/kg dry soil for AMPA, the highest concentrations tested. Soil nitrogen-transformation processes were unaffected by glyphosate and AMPA at 33.1 mg a.e./kg soil and 160 mg/kg soil, respectively. Comparison of these endpoints with worst-case soil concentrations expected for glyphosate (6.62 mg a.e./kg dry soil) and AMPA (6.18 mg/kg dry soil) for annual applications at the highest annual rate of 4.32 kg a.e./ha indicate very low likelihood of adverse effects on soil biota. Environ Toxicol Chem 2016;35:2742-2752. © 2016 The Authors. Environmental Toxicology and Chemistry Published by Wiley Periodicals, Inc. on behalf of SETAC.

Computer simulation of the interactions of glyphosate with metal ions in phloem.

Essential nutrients such as trace metal ions, amino acids, and sugars are transported in the phloem from leaves to other parts of the plant. The major chelating agents in phloem include nicotianamine, histidine, cysteine, glutamic acid, and citrate. A computer model for the speciation of metal ions in phloem has been used to assess the degree to which the widely used herbicide glyphosate binds to Fe(3+), Fe(2+), Cu(2+), Zn(2+), Mn(2+), Ca(2+), and Mg(2+) in this fluid over the pH range of 8 to 6.5. The calculations show that glyphosate is largely unable to compete effectively with the biological chelating agents in phloem. At a typical phloem pH of 8, 1.5 mM glyphosate binds 8.4% of the total Fe(3+), 3.4% of the total Mn(2+), and 2.3% of the total Mg(2+) but has almost no effect on the speciation of Ca(2+), Cu(2+), Zn(2+), and Fe(2+). As the pH decreases to 6.5, there are some major shifts of the metal ions among the biological chelators, but only modest increases in glyphosate binding to 6% for Fe(2+) and 2% for Zn(2+). The calculations also indicate that over 90% of the glyphosate in phloem is not bound to any metal ion and that none of the metal-glyphosate complexes exceed their solubility limits.

A prospective observational study of the clinical toxicology of glyphosate-containing herbicides in adults with acute self-poisoning.

CONTEXT: The case fatality from acute poisoning with glyphosate-containing herbicides is approximately 7.7% from the available studies but these have major limitations. Large prospective studies of patients with self-poisoning from known formulations who present to primary or secondary hospitals are needed to better describe the outcome from acute poisoning with glyphosate-containing herbicides. Furthermore, the clinical utility of the glyphosate plasma concentration for predicting clinical outcomes and guiding treatment has not been determined. OBJECTIVE: To describe the clinical outcomes, dose-response, and glyphosate kinetics following self-poisoning with glyphosate-containing herbicides. METHODS: This prospective observational case series was conducted in two hospitals in Sri Lanka between 2002 and 2007. We included patients with a history of acute poisoning. Clinical observations were recorded until discharge or death. During a specified time period, we collected admission (n = 216, including five deaths) and serial (n = 26) blood samples in patients. Severity of poisoning was graded using simple clinical criteria. RESULTS: Six hundred one patients were identified; the majority ingested a concentrated formulation (36%, w/v glyphosate). Twenty-seven percent were asymptomatic, 63.7% had minor poisoning, and 5.5% of patients had moderate to severe poisoning. There were 19 deaths (case fatality 3.2%) with a median time to death of 20 h. Gastrointestinal symptoms, respiratory distress, hypotension, altered level of consciousness, and oliguria were observed in fatal cases. Death was strongly associated with greater age, larger ingestions, and high plasma glyphosate concentrations on admission (>734 microg/mL). The apparent elimination half-life of glyphosate was 3.1 h (95% CI = 2.7-3.6 h). CONCLUSIONS: Despite treatment in rural hospitals with limited resources, the mortality was 3.2%, which is lower than that reported in previous case series. More research is required to define the mechanism of toxicity, better predict the small group at risk of death, and find effective treatments.

Investigation of the mechanism of chlorination of glyphosate and glycine in water.

The chlorination reactions of glyphosate and glycine in water were thoroughly studied. Utilizing isotopically enriched (13C and 15N) samples of glycine and glyphosate and 1H, 13C, 31P, and 15N NMR spectroscopy we were able to identify all significant terminal chlorination products of glycine and glyphosate, and show that glyphosate degradation closely parallels that of glycine. We have determined that the C1 carboxylic acid carbon of glycine/glyphosate is quantitatively converted to CO2 upon chlorination. The C2 methylene carbon of glycine/glyphosate is converted to CO2 and methanediol. The relative abundance of these two products is a function of the pH of the chlorination reactions. Under near neutral to basic reaction conditions (pH 6-9), CO2 is the predominant product, whereas, under acidic reaction conditions (pH < 6) the formation of methanediol is favored. The C3 phosphonomethylene carbon of glyphosate is quantitatively converted to methanediol under all conditions tested. The nitrogen atom of glycine/glyphosate is transformed into nitrogen gas and nitrate, and the phosphorus moiety of glyphosate produces phosphoric acid upon chlorination. In addition to these terminal chlorination products, a number of labile intermediates were also identified including N-chloromethanimine, N-chloroaminomethanol, and cyanogen chloride. The chlorination products identified in this study are not unique to glyphosate and are similar to those expected from chlorination of amino acids, proteins, peptides, and many other natural organic matters present in drinking water.

Chlorination kinetics of glyphosate and its by-products: modeling approach.

Chlorination reactions of glyphosate, glycine, and sodium cyanate were conducted in well-agitated reactors to generate experimental kinetic measurements for the simulation of chlorination kinetics under the conditions of industrial water purification plants. The contribution of different by-products to the overall degradation of glyphosate during chlorination has been identified. The kinetic rate constants for the chlorination of glyphosate and its main degradation products were either obtained by calculation according to experimental data or taken from published literature. The fit of the kinetic constants with experimental data allowed us to predict consistently the concentration of the majority of the transitory and terminal chlorination products identified in the course of the glyphosate chlorination process. The simulation results conducted at varying aqueous chlorine/glyphosate molar ratios have shown that glyphosate is expected to degrade in fraction of a second under industrial aqueous chlorination conditions. Glyphosate chlorination products are not stable under the conditions of drinking water chlorination and are degraded to small molecules common to the degradation of amino acids and other naturally occurring substances in raw water. The kinetic studies of the chlorination reaction of glyphosate, together with calculations based on kinetic modeling in conditions close to those at real water treatment plants, confirm the reaction mechanism that we have previously suggested for glyphosate chlorination.