GLYPHOSATE
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
Glycine, N-(phosphonomethyl)- Glyphosate MON 0573 MON 2139 N-Phosphonomethyl glycine N-(Phosphonomethyl)glycine Herbicides, Glyphosate
IDENTIFIERS
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
C3H8NO5P HOOCCH2NHCH2PO(OH)2
SYNONYM REFERENCE
- (EPA, 2005; HSDB, 2004; NLM, 2004; RTECS, 2004; Pohanish, 2002; Lewis, 2000)
USES/FORMS/SOURCES
Glyphosate is formulated into systemic herbicides that provide non-selective, post-emergent control of annual and perennial plants. The herbicide product is extensively used because of its suitability for general weed control on many food and non-food crops (forests, nurseries), on "no-till" farmland, on non-cropland (industrial, recreational, public areas), in aquaculture, and for aquatic weed control in reservoirs (HSDB, 2004; Meister, 2003; Pohanish, 2002; EPA, 2002). Technical grade glyphosate (glyphosate acid, CAS 1071-83-6), as the pure chemical by itself, is not directly applied as a herbicide in the environment, nor is it included in product formulations. Rather, it is the isopropylamine (IPA) salt form of glyphosate that is formulated into most commercial products (Tsui & Chu, 2003; Krieger, 2001).
Glyphosate is an odorless, colorless to white crystalline powder. It is a weak acid and zwitterionic (dipolar ion) with dissociation constants (pKa) that range from less than 2 to 10.6. As a 1% solution, it has a pH of 2 (HSDB, 2004; Pohanish, 2002; Krieger, 2001). Glyphosate's technical purity grade is generally greater than 90% (averaging 96% purity on a dry weight basis). The minimum purity for technical grade glyphosate is 80% (HSDB, 2004; Krieger, 2001; IPCS, 1994). Glyphosate herbicides are commonly applied in spray form and primarily formulated as either a water-soluble liquid or concentrate solution, or a solution made with a water-soluble powder and other ingredients. Glyphosate herbicides also come as pressurized liquids, aerosols, emulsions, pellets/tablets, granules, powders, and microencapsulated products (Meister, 2003; Giesy et al, 2000; Krieger, 2001; EPA, 2002; Harbison, 1998). Glyphosate herbicides commonly consist of water and the isopropylamine (IPA) salt form (CAS 38641-94-0) of glyphosate, or they include water, the IPA salt, plus a surfactant and other inert ingredients. Commercial herbicides may contain other glyphosate salts (trimethylsulfonium, monoammonium, and sodium) as the active ingredient (HSDB, 2004; Pohanish, 2002; Giesy et al, 2000; EPA, 2002). Glyphosate formulations and their toxicity differ depending on the type and concentration of the active ingredient and/or the added surfactants. The polyoxyethylene tallowamines (e.g., polyoxyethylene amine or POEA) is a class of surfactants most commonly used in glyphosate formulations. Other glyphosate herbicide additives include sulfuric and phosphoric acid and a variety of inert materials (HSDB, 2004; Giesy et al, 2000; EPA, 2002).
SOURCES OF EXPOSURE OCCUPATIONAL Potential occupational exposure to glyphosate exists for those involved in its manufacture, as well as the formulation and application of glyphosate herbicides. Worker exposure may occur during spraying, mixing, and cleaning. Potential exposure routes include inhalation, ingestion, and/or skin contact with the chemical or with plants and soil that have been sprayed. Worker exposure may also occur during transport, storage, and disposal of this chemical (HSDB, 2004; EPA, 2002; Pohanish, 2002).
GENERAL POPULATION The general public may be exposed to glyphosate, given its widespread use for control of terrestrial and aquatic weeds in residential and recreational areas (parks, golf courses, and reservoirs). Potential exposure routes for swimmers in treated reservoirs include dermal contact and incidental ingestion (69 FR 51301 - 51312, 2004; HSDB, 2004; Pohanish, 2002). Gardeners may be exposed to glyphosate through contact with or use of a variety of commercial herbicide products containing this chemical or through contact with treated plants (HSDB, 2004). Dermal and dietary exposure is possible for persons intentionally or accidentally touching or consuming food and water that have been recently sprayed (HSDB, 2004; Pohanish, 2002).
COMMERCIAL PRODUCTION Production of glyphosate is a two-phase process. First, a mixture of glycine (50 parts), chloromethylphosphonic acid (92 parts), an aqueous solution of 50% sodium hydroxide (150 parts), and water (100 parts) are refluxed. Additional aqueous solution of 50% sodium hydroxide (50 parts) is added to maintain basic pH and refluxing is resumed. Then, the mixture is cooled and filtered before concentrated hydrochloric acid (160 parts) is added and the mixture is filtered again. Glyphosate is slowly precipitated out in the filtrate (IPCS, 1994).
COMMERCIAL SOURCES Glyphosate-based herbicide formulations are sold under many tradenames and produced by numerous manufacturers. Glyphosate was first introduced as a commercial product in 1974. Glyphosate production and its use in commercial herbicides for agriculture continues to increase worldwide (Meister, 2003; Krieger, 2001).
SYNONYM EXPLANATION
- Editor's note: Many of the references used do not clearly distinguish between technical grade glyphosate (CAS 1071-83-6) and the isopropylamine (IPA) salt form of glyphosate (CAS 38641-94-0) commonly used in commercial formulations. This is the case for synonyms and tradenames, as well as for toxicity listings and physical properties. Throughout this document, an effort was made to indicate whether the information was related to the pure chemical, a salt form, or a product formulation.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Glyphosate is a broad-spectrum systemic herbicide, and is the most widely used herbicide in the USA. It is available under a variety of trade names, including Roundup(R).
- TOXICOLOGY: Glyphosate is an aminophosphonic analogue of the amino acid glycine. It kills plants by interfering with the synthesis of the amino acids phenylalanine, tyrosine, and tryptophan. Other chemicals added to glyphosate mixtures (eg, surfactants and diquat) are probably responsible for much of the reported toxicity.
- EPIDEMIOLOGY: Exposure is common, severe toxicity is rare. In the United States, poison centers in the past decade have reported more than 4000 exposures per year of glyphosate-containing herbicides, of which several hundred are evaluated in a healthcare facility. However, only about 1% of these exposures were intentional ingestions, and fatalities are rare. The clinical effects described are limited to glyphosate isoprophylamine (also known as Roundup(R)) and not glyphosate-trimesium, which appears to have a different mechanism of action that may produce rapid toxicity following ingestion. Two fatal cases of intoxication have been reported within 1 hour or less of oral exposure in an adult and a child to glyphosate-trimesium
MILD TO MODERATE TOXICITY: Ingestion can cause nausea, vomiting, abdominal pain, diarrhea, slight sedation, mouth and throat pain. Eye exposure can cause conjunctivitis. Dermal exposure can cause erythema, piloerection, and contact dermatitis. SEVERE TOXICITY: Oral or gastrointestinal mucosal ulceration, hypotension, mild elevations in liver enzymes, leukocytosis, metabolic acidosis, oliguric/anuric renal failure, hyperthermia, pulmonary edema, respiratory failure, ventricular dysrhythmias, coma, and seizures are rare manifestations generally only seen after deliberate ingestion. Severe toxicity resulting in death, most often following intentional exposure, has been related to hypovolemic shock followed by respiratory failure. Prolonged dermal exposure can cause burns. The development of respiratory distress, pulmonary edema, renal failure or acidosis requiring hemodialysis, and/or hyperkalemia are highly associated with poor prognosis.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Inhalation of material may be harmful. Contact may cause burns to skin and eyes. Inhalation of Asbestos dust may have a damaging effect on the lungs. Fire may produce irritating, corrosive and/or toxic gases. Some liquids produce vapors that may cause dizziness or suffocation. Runoff from fire control may cause pollution.
ACUTE CLINICAL EFFECTS
USES: Glyphosate is a broad-spectrum systemic herbicide, and is the most widely used herbicide in the USA. It is available under a variety of trade names, including Roundup(R). TOXICOLOGY: Glyphosate is an aminophosphonic analogue of the amino acid glycine. It kills plants by interfering with the synthesis of the amino acids phenylalanine, tyrosine, and tryptophan. Other chemicals added to glyphosate mixtures (eg, surfactants and diquat) are probably responsible for much of the reported toxicity. EPIDEMIOLOGY: Exposure is common, severe toxicity is rare. In the United States, poison centers in the past decade have reported more than 4000 exposures per year of glyphosate-containing herbicides, of which several hundred are evaluated in a healthcare facility. However, only about 1% of these exposures were intentional ingestions, and fatalities are rare. PRODUCT VARIABILITY: The clinical effects described are limited to glyphosate isoprophylamine (also known as Roundup(R)) and not glyphosate-trimesium, which appears to have a different mechanism of action that may produce rapid toxicity following ingestion. Two fatal cases of intoxication have been reported within 1 hour or less of oral exposure in an adult and a child to glyphosate-trimesium (Sorensen & Gregersen, 1999).
MILD TO MODERATE TOXICITY: Ingestion can cause nausea, vomiting, abdominal pain, diarrhea, slight sedation, mouth and throat pain. Eye exposure can cause conjunctivitis. Dermal exposure can cause erythema, piloerection, and contact dermatitis. SEVERE TOXICITY: Oral or gastrointestinal mucosal ulceration, hypotension, mild elevations in liver enzymes, leukocytosis, metabolic acidosis, oliguric/anuric renal failure, hyperthermia, pulmonary edema, respiratory failure, ventricular dysrhythmias, coma, and seizures are rare manifestations generally only seen after deliberate ingestion. Severe toxicity resulting in death, most often following intentional exposure, has been related to hypovolemic shock followed by respiratory failure. In one study, the volume of surfactant not the type surfactant had a role in the development of hypotension, mental deterioration, respiratory failure, acute kidney injury and arrhythmia. Prolonged dermal exposure can cause burns. The development of respiratory distress, pulmonary edema, renal failure or acidosis requiring hemodialysis, and/or hyperkalemia are highly associated with poor prognosis. Deaths following the ingestion of glyphosate have occurred. The average amount of the 41% solution of glyphosate herbicide ingested by nonsurvivors was 184 +/- 70 mL (range, 85 to 200 mL); however, amounts up to 500 mL have been survived with only mild to moderate symptoms (Talbot et al, 1991). Pulmonary edema, metabolic acidosis, and hyperkalemia are predictors highly associated with poor outcome and mortality in a retrospective case series (n=131). Renal failure necessitating hemodialysis is also indicative of a poor prognosis (Lee et al, 2000).
Hypotension and signs of hypovolemic shock have been reported following acute ingestions (Chen et al, 1995; Talbot et al, 1991; Tominack et al, 1991; Sawada et al, 1988). In severe poisonings, oliguria and anuria may be secondary to hypotension. In one series, 18 (18.5%) of 97 patients who ingested a 41% concentration of glyphosate developed shock (Tominack et al, 1991).
Acute lung injury has been reported in up to 13% of individuals orally exposed to glyphosate (Tominack et al, 1991) Pulmonary edema along with metabolic acidosis, and hyperkalemia were highly predictive of poor outcome and mortality in a retrospective case series (n=131) (Sawada & Nagai, 1987). In another case series, aspiration pneumonia was found to be the major cause of mortality (Chang et al, 1999).
Mental status changes have developed in 11% to 12% of patients following acute ingestion, and may be secondary to hypoxia or hypotensive effects (Talbot et al, 1991; Tominack et al, 1991)
Nausea, vomiting, erythema of the mucous membranes, and epigastric pain are common findings following ingestion; paralytic ileus can develop in severe cases. Chemical burns of the esophagus and gastric region have been reported (Sawada & Nagai, 1987). Although reported less frequently, diarrhea can be moderate to severe, and produce alterations in fluid and electrolyte balance (Tominack et al, 1991).
ORAL: Analysis of 3 retrospective reviews with a total of 246 cases of ingestion of a commercial product containing glyphosate 41% and polyoxyethyleneamine surfactant 15% highlight the following signs and symptoms (Tominack et al, 1991; Talbot et al, 1991; Sawada et al, 1988) : Oral and throat pain 41% to 43% Oral mucosal ulceration/erosion 7% to 43% Vomiting 44%; Diarrhea 12% Abnormal mental status 11% to 12% Oliguria/Anuria 10% to 14% Metabolic Acidosis 14% Hyperthermia 7% Pulmonary edema 5% to 13% Mild LFT elevation 19% to 40% Leukocytosis 52% to 78% Shock 9%
INHALATION: Based on limited data, inhalation of glyphosate produced pneumonitis in one worker (Carel & Pushnoy, 1999). This study has been refuted (Goldstein et al, 1999). DERMAL: Commercial grade formulations have resulted in erythema and contact dermatitis (Moses, 1989a; CDFA, 1984). Based on studies on unabraded skin, dilute glyphosate products showed no greater irritation potential than all purpose cleaners. Skin sensitization was not observed, nor any potential for photoirritation or photosensitization. Testing on abraded skin can result in mild irritation and erythema (HSDB, 2004). CASE REPORT: Approximately 24 hours after exposure, extensive chemical burns resulting in erythematous macules and areas of necrotic erosion occurred in a 78-year-old woman following prolonged cutaneous contact with glyphosate. Following supportive care (ie, wet dressings, topical steroid therapy, and systemic antibiotics), clinical improvement was observed within 1 week and complete resolution occurred at 4 weeks (Amerio et al, 2004). In one study, accidental dermal exposure was asymptomatic (HSDB, 2004).
OCULAR: Following accidental ocular exposure, gross periorbital edema with chemosis of the eye developed in conjunction with tachycardia, palpitations, and hypertension. Treatment with intramuscular promethazine resolved the symptoms within 24 hours (Temple & Smith, 1992).
CHRONIC CLINICAL EFFECTS
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
- PREHOSPITAL: Small amounts of water may be used for dilution after ingestion. Wash exposed skin, irrigate exposed eyes and remove contaminated clothing. Activated charcoal in general should be avoided.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves.
DERMAL EXPOSURE EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE Emesis is NOT recommended, although spontaneous vomiting may occur. The concentrated solution (41% glyphosate) may cause esophageal erosion; it is not known if lower concentrations are less irritating or if the surfactant is an irritant. Rinse the mouth and dilute with milk or water. For smaller ingestions, oral irrigation and dilution may be all that is necessary. If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. The exact ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004). USE OF DILUENTS IS CONTROVERSIAL: While experimental models have suggested that immediate dilution may lessen caustic injury (Homan et al, 1993; Homan et al, 1994; Homan et al, 1995), this has not been adequately studied in humans. DILUENT TYPE: Use any readily available nontoxic, cool liquid. Both milk and water have been shown to be effective in experimental studies of caustic ingestion (Maull et al, 1985; Rumack & Burrington, 1977; Homan et al, 1995; Homan et al, 1994; Homan et al, 1993). ADVERSE EFFECTS: Potential adverse effects include vomiting and airway compromise (Caravati, 2004). CONTRAINDICATIONS: Do NOT attempt dilution in patients with respiratory distress, altered mental status, severe abdominal pain, nausea or vomiting, or patients who are unable to swallow or protect their airway. Diluents should not be force fed to any patient who refuses to swallow (Rao & Hoffman, 2002). ACTIVATED CHARCOAL Do not administer activated charcoal to patients who are already vomiting or have evidence of caustic injury. PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002). In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis. The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
GENERAL Systemic effects of acute ingestion can include: hypotension, shock, pulmonary edema, and metabolic acidosis.
HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response. ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
INHALATION EXPOSURE At the time of this review, glyphosate has low toxicity when inhaled. INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
- FATAL PROGNOSTIC INDICATORS
The mean amount of concentrated Roundup(R) (40% glyphosate) ingested in 9 fatal cases was 206 mL (Sawada et al, 1988). These cases were all deliberate suicidal ingestion. CASE REPORT: A 37-year-old woman died after ingesting approximately 500 mL of glyphosate as Roundup(R) (the formulation contained 41% glyphosate as the isopropylamine salt and 15% polyoxyethylene amine as a surfactant). At autopsy, there was evidence of gastrointestinal hemorrhage, pulmonary and brain edema and liver toxicity. A toxicology screen was negative (Sribanditmongkol et al, 2012). CASE REPORT: A 25-year-old woman was admitted with a 4 day history of fever and painful oral ulcers after intentionally ingesting glyphosate. Physical exam showed extensive oral ulcers that bled easily. By day 3, it was determined that she had ingested 100 to 150 mL of glyphosate (43.15% w/w with 95% purity and net concentration of 41% SL) after developing subcutaneous emphysema and pneumomediastinum due to esophageal perforation. Her clinical course rapidly declined requiring mechanical ventilation, inotropes and dialysis. She died 12 days after ingestion (Jyoti et al, 2014). Ingestion of approximately 50 mL of a glyphosate-trimesium herbicide formulation by a 6-year-old boy resulted in death within minutes. A 34-year-old woman who ingested approximately 150 mL of a glyphosate-trimesium herbicide also died quickly. Findings on postmortem examination included pulmonary edema, erosion of gastric mucous membranes, cerebral edema, and dilated right atrium and ventricle of the heart (Sorensen & Gregersen, 1999). MORTALITY CASE FATALITY RATE: The fatality rate in 67 cases of Roundup(R) poisoning was 7.5%, and the average dose was 184 +/- 70 mL (range 85 to 200 mL). All fatal cases were suicidal ingestions. Ingestion of larger, nonfatal doses (500 mL) was reported for some patients (Talbot et al, 1991). In a series of 97 adult ingestion cases (ages 12 to 77), mortality was 17%. Most (88%) were suicidal attempts (Tominack et al, 1991). In a series of 22 adult suicidal ingestion cases, 4 patients (18%) died (Sheu et al, 1998). In a retrospective case series (n=131) of glyphosate-surfactant poisonings, patients that ingested greater than 200 mL were at increased risk of death (Lee et al, 2000). In a series of 601 glyphosate ingestions there were 19 fatalities. Fatal cases had ingested 75 mo to 350 ml concentrated glyphosate (generally 36% w/v) (Roberts et al, 2010).
MAXIMUM TOLERATED EXPOSURE
No deaths occurred with a history of ingestion of less than 150 mL concentrate or in patients less than 40 years of age (Tominack et al, 1991). The manufacturer reports that ingestions of 1 to 8 ounces (30 to 240 mL) of concentrate resulted in vomiting and diarrhea of 2 to 5 days duration, but no other symptoms. Sawada et al (1988) reported that 47 patients who ingested a mean of 104 mL developed significant symptoms (co-ingestants not reported) (Sawada et al, 1988). A 69-year-old woman intentionally ingested 500 mL of glyphosate-surfactant herbicide (48% glyphosate potassium salts; Roundup Maxload (R)) and was found alert but vomiting by her spouse. Once admitted, she lost consciousness and became pulseless. Following CPR and repeated cardioversion; ventricular tachycardia was unresponsive to antiarrhythmics. Initial laboratory findings included severe hyperkalemia (potassium 10 mEq/L), normal renal function and metabolic acidosis. Treatment included percutaneous cardiopulmonary support and continuous hemodialysis which corrected the patient's elevated potassium concentration. The patient recovered following a complicated clinical course that included esophageal and gastric erosions and acute respiratory distress syndrome. The patient required intubation and mechanical ventilation for 20 days. Her serum glyphosate concentration on admission was 1625.74 mcg/mL and 18 hours later was 100.44 mcg/mL (Kamijo et al, 2012). A 51-year-old man developed multiorgan system damage, including acute renal failure with oliguria and severe hypoxia, 12 hours after ingesting "4 gulps" (approximately 240 mL) of a product that contained 18% glyphosate, 0.73% diquat, and 7% polyoxyethyleneamine (POEA). After supportive therapy, including 4 hours of hemodialysis, the patient's status improved and he gradually regained renal function (Sampogna & Cunard, 2007).
CASE REPORT: A 22-year-old man survived after self-injecting approximately 250 mL of diluted glyphosate-surfactant herbicide in a suicide attempt. The patient presented with mild metabolic acidosis and acute hemolysis, which required plasmapheresis and blood transfusions. He made a full recovery 4 days later (Wu et al, 2006).
In a retrospective review of 107 patients with acute glyphosate intoxication, surfactant volume had a role in the development of severe toxicity compared to the surfactant type (ingredient) in various glyphosate herbicide products. In patients that ingested surfactant volumes of 8 mL or more there was a strong association with the development of hypotension (47.1%), mental deterioration (38.6%), respiratory failure (30%), acute kidney injury (17.1%) and arrhythmia (10%). Most patients improved with no long-term sequelae; however, 2 patients died of refractory shock, metabolic acidosis and respiratory failure (Seok et al, 2011).
- Carcinogenicity Ratings for CAS1071-83-6 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Glyphosate IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): 2A ; Listed as: Glyphosate 2A : The agent (mixture) is probably carcinogenic to humans. The exposure circumstance entails exposures that are probably carcinogenic to humans. This category is used when there is limited evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals. In some cases, an agent (mixture) may be classified in this category when there is inadequate evidence of carcinogenicity in humans and sufficient evidence of carcinogenicity in experimental animals and strong evidence that the carcinogenesis is mediated by a mechanism that also operates in humans. Exceptionally, an agent, mixture or exposure circumstance may be classified in this category solely on the basis of limited evidence of carcinogenicity in humans.
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS1071-83-6 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 1x10(-1) mg/kg-day
Inhalation: Drinking Water:
LOAEL- (ORAL)MOUSE: LOAEL- (INHALATION)RAT: LOAEL- (ORAL)RAT: NOAEL- (ORAL)HUMAN: UNASSIGNED- (ORAL)HUMAN:
CALCULATIONS
To convert between glyphosate acid equivalents (a.e.), glyphosate active ingredients (a.i.), and concentrations in glyphosate herbicides like Roundup(R), one may assume the following (Giesy et al, 2000): 1 mg Roundup(R) = 0.31 mg glyphosate acid equivalents (a.e.) 1 mg of glyphosate active ingredient (a.i.) = 0.75 glyphosate a.e. The glyphosate concentration in Roundup(R) is typically 360 gm-a.e./L or less (e.g., 240, 160, 120, 9 gm-a.e./L). The standard Roundup(R) formulation of 360 gm (glyphosate) a.e./L = 0.75 lb glyphosate a.e./qt or 1.0 lb glyphosate a.i./qt.
OTHER CONVERSION FACTORS 1 ppm = 6.91 mg/m(3) at 25 degrees Celsius and 101.3 kPa (IPCS, 1994) 1 mg/m(3) = 0.145 ppm (IPCS, 1994)
The purity for technical grade glyphosate is generally >90% (96% purity (dry wt basis). The minimum purity for technical grade glyphosate is 80% (HSDB, 2004; Krieger, 2001).
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS1071-83-6 (American Conference of Governmental Industrial Hygienists, 2010):
- AIHA WEEL Values for CAS1071-83-6 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS1071-83-6 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS1071-83-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS1071-83-6 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS1071-83-6 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS1071-83-6 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS1071-83-6 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS1071-83-6 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS1071-83-6 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS1071-83-6 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS1071-83-6 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS1071-83-6 (NFPA, 2002):
-HANDLING AND STORAGE
HANDLING
- Wear appropriate, splash-proof, chemical protective clothing and equipment to prevent dermal and eye contact, inhalation, or ingestion of glyphosate solids (dusts), liquid, and mists/vapors (HSDB, 2004; Pohanish, 2002; ILO ICSC, 2000).
- Wash thoroughly with soap and water after handling glyphosate material (Pohanish, 2002; ILO ICSC, 2000).
- Do not handle or store glyphosate around drinking water, food, or agricultural feedstuffs (HSDB, 2004; Meister, 2003; ILO ICSC, 2000).
STORAGE
Store glyphosate solutions in synthetic, plastic, fiberglass, or aluminum containers. Do not store glyphosate in iron or galvanized steel (or unlined steel) containers, which glyphosate solutions can corrode. Follow manufacturer's container and storage recommendations for specific glyphosate products (HSDB, 2004; Pohanish, 2002; ILO ICSC, 2000). Keep glyphosate away from ignition sources; store containers in a cool, dry, and well-ventilated location (Pohanish, 2002; ILO ICSC, 2000). Store glyphosate away from potable water and food items, as well as agricultural feed and seed (Meister, 2003; ILO ICSC, 2000).
Glyphosate can corrode iron and galvanized steel containers and subsequently form combustible and explosive gas mixtures (Pohanish, 2002; ILO ICSC, 2000). Store containers of glyphosate separated from oxidizers (Pohanish, 2002).
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
- Prevent eye and skin contact to glyphosate through use of appropriate personal protective clothing and equipment, including chemical-protective gloves, overclothing, and chemical safety goggles. Minimize inhalation of glyphosate dusts, spray mist, and vapors through use of adequate respiratory protection. Immediately remove any clothing that becomes wet or contaminated to prevent any dermal contact (Meister, 2003; Pohanish, 2002; ILO ICSC, 2000).
EYE/FACE PROTECTION
- Wear chemical-protective goggles or face shield when working with or around glyphosate. Avoid wearing contact lenses around this chemical (Pohanish, 2002; ILO ICSC, 2000).
- Avoid bodily contact with glyphosate (Pohanish, 2002; ILO ICSC, 2000).
RESPIRATORY PROTECTION
- Avoid inhalation of glyphosate dust, spray mist, particulate, and vapors by using appropriate respiratory protection (Pohanish, 2002; ILO ICSC, 2000).
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 1071-83-6.
OTHER
- INDUSTRIAL DECONTAMINATION
Emergency showers and eye wash stations should be present in areas where glyphosate is used (Pohanish, 2002). If glyphosate contacts the skin, promptly wash the the affected area(s) with water or soap and water; seek prompt medical attention as required (Pohanish, 2002; ILO ICSC, 2000). In case of eye contact, remove contacts if present, and flush eyes with copious amounts of water for a minimum of 15 minutes; seek medical attention (Pohanish, 2002; ILO ICSC, 2000). In case of inhalation, move victim to fresh air and seek immediate medical attention (Pohanish, 2002; ILO ICSC, 2000). In case of ingestion, seek immediate medical attention (ILO ICSC, 2000). Immediately remove any contaminated clothing and then wash body thoroughly with soap and water (Pohanish, 2002; ILO ICSC, 2000).
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) Some may burn but none ignite readily. Containers may explode when heated. Some may be transported hot.
The solid form of glyphosate is combustible and may burn under specific conditions, but it does not readily ignite (Pohanish, 2002; ILO ICSC, 2000). Water-based formulations of glyphosate are not flammable (HSDB, 2004; Tomlin, 2000). The corrosive reaction of glyphosate solutions with iron or steel (unlined or galvanized) may produce highly combustible, explosive gas mixtures (Pohanish, 2002). High temperatures from fire may cause glyphosate decomposition and the release of toxic fumes (oxides of nitrogen and phosphorous) (Tomlin, 2000).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS1071-83-6 (NFPA, 2002):
- INITIATING OR CONTRIBUTING PROPERTIES
Storage of glyphosate solutions in iron, galvanized steel, or unlined steel containers may result in hazardous corrosive reactions (Pohanish, 2002; ILO ICSC, 2000).
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Do not scatter spilled material with high pressure water streams. Dike fire-control water for later disposal.
- TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire.
- NFPA Extinguishing Methods for CAS1071-83-6 (NFPA, 2002):
- Use dry chemical, carbon dioxide, alcohol-resistant foam or water spray to control fires involving glyphosate (Pohanish, 2002; ILO ICSC, 2000).
- Runoff or dilution water resulting from fire control may be toxic or corrosive and should be controlled (ILO ICSC, 2000).
When heated to decomposition, glyphosate releases toxic and irritating fumes of nitrogen oxides and phosphorous oxides (Pohanish, 2002; ILO ICSC, 2000; Lewis, 2000).
EXPLOSION HAZARD
- Contact of glyphosate solutions with iron or steel (unlined or galvanized) may produce highly explosive, combustible gas mixtures (Pohanish, 2002).
- Glyphosate and its salts are ordinarily stable in air (Tomlin, 2000).
DUST/VAPOR HAZARD
- Avoid exposure (ingestion, inhalation, dermal contact) with glyphosate dust, mist, and vapors, as they are eye, skin, and respiratory irritants (Pohanish, 2002; ILO ICSC, 2000).
REACTIVITY HAZARD
- Glyphosate solutions can corrode and react with iron and galvanized steel to produce combustible, explosive gas mixtures (Pohanish, 2002).
- The reactivity hazards and physical properties of different glyphosate formulations vary depending on the ingredients (ILO ICSC, 2000).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171(ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind.
- Evacuate unnecessary persons to a safe location upwind of the spill area. Prevent inhalation or ingestion of, or direct contact with of the spilled material in any form (solid, particulate, aerosols, vapors) (Pohanish, 2002; ILO ICSC, 2000)
- AIHA ERPG Values for CAS1071-83-6 (AIHA, 2006):
- DOE TEEL Values for CAS1071-83-6 (U.S. Department of Energy, Office of Emergency Management, 2010):
- AEGL Values for CAS1071-83-6 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS1071-83-6 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent dust cloud. Avoid inhalation of asbestos dust.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) Wear appropriate protective clothing and respiratory equipment to avoid direct contact, inhalation, and ingestion of spilled glyphosate. Remove all ignition sources and ventilate the spill area. Prevent spills from entering sewers or water intakes (Pohanish, 2002; ILO ICSC, 2000).
SMALL SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) SMALL DRY SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) Wear appropriate protective clothing and respiratory equipment to prevent inhalation, ingestion, or direct skin contact with glyphosate (Pohanish, 2002; ILO ICSC, 2000). Moisten powdered glyphosate prior to collecting and placing the material into plastic containers (Pohanish, 2002; ILO ICSC, 2000). Use sand or inert absorbent to cleanup spilled liquid. Collect absorbant and spilled liquid in sealable containers (Pohanish, 2002; ILO ICSC, 2000).
Mix glyphosate with excess calcium oxide or sodium hydroxide and sand or other adsorbent. When calcium oxide is used, sodium carbonate may be added to increase the rate of reaction. The total amount of alkali required will depend on the volume and concentration of glyphosate. To ensure chemical interactions are not too vigorous, it is advisable to run a small preliminary batch before proceeding to dispose of the entire quantity (HSDB, 2004). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Glyphosate is released to the environment through its common use as an herbicide spray for controlling terrestrial and aquatic weeds. Glyphosate herbicides can enter terrestrial and aquatic environments through targeted or accidental spraying, or as surface runoff or spray drift. Organisms may be exposed by dermal and dietary exposure routes from touching or consuming food or water that have been directly sprayed or exposed by spray drift (HSDB, 2004; Pohanish, 2002; EPA, 2002; Verschueren, 2001).
- Glyphosate herbicides are widely used in residential and recreational areas (e.g., parks, golf courses, reservoirs) to control both terrestrial and aquatic weeds (HSDB, 2004; Pohanish, 2002).
- People may be exposed to glyphosate through their use of commercial products containing the chemical (commonly in its salt form) or by direct contact with plants that have been sprayed (HSDB, 2004; EPA, 2002).
ENVIRONMENTAL FATE AND KINETICS
Glyphosate is mainly released into the atmosphere through use of herbicide sprays, which commonly contain glyphosate in its isopropylamine (IPA) salt form. Glyphosate is non-volatile and exists only as an aerosol in the atmosphere, where it primarily degrades by photolysis or by gravitational settling. It is generally stable to photodegradation and hydrolysis (at pH 3, 6, and 9, and at 5-35 degrees C) (HSDB, 2004; EPA, 2002; Tomlin, 2000). Vaporization from soil and plant surfaces is an insignificant transport pathway for glyphosate, given glyphosate's negligible vapor pressure (HSDB, 2004; Giesy et al, 2000). Glyphosate can photodegrade in the presence of UV radiation, but not visible light. Glyphosate's physical state as a free molecule or a tightly-bound complex affects its photodegradation potential (HSDB, 2004).
SURFACE WATER Adsorption to sediment or particulate matter and biodegradation are the principal means for glyphosate removal from the water column. Higher residue levels are associated with sediments and suspended sediments, as glyphosate readily forms insoluble complexes with metal ions which then precipitate out of the water column (HSDB, 2004; Perkins et al, 2000). Glyphosate (the alkali metal and amine salt forms) is readily soluble in water. Dilution and dispersion contribute to glyphosate's dissipation in flowing water systems (HSDB, 2004; Giesy et al, 2000).
Reported residue reduction levels and half-life data for glyphosate in aquatic ecosystems systems include the following (HSDB, 2004): A half-life range of 1.51-1.99 days in three Canadian forest ponds, with a residue reduction of 100% (not detected) at 38 days. Glyphosate's half-life was longer in the pond that had higher calcium and magnesium levels. A stormwater peak concentration of 0.28 ppm on aerially treated forest-brush land along the Oregon coast was detected shortly after application. Six days following application, glyphosate was not detectable. Residue reduction in flowing water in two irrigation canals were 13%/km and 27%/km, with corresponding benthic sediment uptake rates of 365 and 603 g/km, respectively. A peak sediment concentration of 0.55 ppm occurred at 14 days after treatment, followed by a decline to approximately 0.1 ppm at 55 days.
Glyphosate dissipates rapidly in stillwater (lentic) lakes and ponds (Perkins et al, 2000). Glyphosate herbicide application at the highest recommended rates (8.9 L/ha for common surfactant-free products and 12 L/ha for common products that contain surfactants) to water 15 cm deep produced an estimated glyphosate acid equivalent (IPA salt) concentration of 2.88 mg/L (Perkins et al, 2000). Glyphosate does not readily elute from sediment. One study showed canal sediment retained >93% of the glyphosate applied 4 days earlier, before the canal was filled with water. In a soil column elution study, no detectable glyphosate was in the leachate at 45 days (HSDB, 2004). Studies on glyphosate photodegradation in aqueous solutions report the following: Photolysis by sunlight of a 1% glyphosate solution in distilled water produced 75% degradation after 2 weeks. Only 15% was degraded in polluted water after 2 weeks (Verschueren, 2001). Researchers calculated an aqueous dissipation half-life of 7.5 days for glyphosate applied to a pond (EPA, 2002). Degradation by direct photolysis in water and sunlight was 0% at 31 days, with an estimated dissipation half-life of 413 days (Verschueren, 2001).
GROUND WATER Iron, copper, calcium, and magnesium ions commonly form insoluble complexes with glyphosate in groundwater and some surface waters. These complexes typically precipitate out of the water column and into sediment (HSDB, 2004). One Texas study reported glyphosate detections in groundwater (HSDB, 2004).
TERRESTRIAL Glyphosate is strongly adsorbed by many soil types. Leachability and mobility in soils are limited by such environmental conditions as soil type, pH, temperature, precipitation, phosphate levels, organic matter content, microbial activity, clay content, cation exchange capacity, and metal ion concentrations (HSDB, 2004; Verschueren, 2001; Giesy et al, 2000; EPA, 2002). Glyphosate has an average half-life of 60 days in soil, according to literature surveys and field study data. Reported residue persistence and half-life data for glyphosate in soil ecosystems include the following (HSDB, 2004): A half-life of 24 days for sandy soils in a Canadian boreal forest, with a residue reduction of >90% at 78 days. Half-lives of 40.2 and 29.2 days on bare soil and litter-covered soil, respectively. A half-life range of 45-60 days for residue dissipation in soils from a coastal forest ecosystem with 82-94% residue reduction at 360 days. A half-life range of 69-127 days on two Finnish crop fields. The field with loam soil had residue reduction levels of 24% and 90% after 28 days and 8 months, respectively. The field with fine silt soil had residue reductions of 8% and 47% at 28 days and 8 months, respectively. Half-lives of 3, 27, and 130 days in Ray silt loam, Drummer silty clay loam, and Norfolk loam soils, respectively (greenhouse study). An average residue reduction of 80% in Swedish forest soils after 9 months (August to May). Retention of >90% glyphosate residues in the 0-15 cm organic soil layer of a British Columbia coastal forest in both the seasonally flooded and well-drained soils.
Glyphosate's half-life ranged from 1.7-142 days (median of 14.9 days) in a bare ground soil study (Verschueren, 2001). Reported residue persistence and dissipation data for glyphosate in terrestrial plant ecosystems include the following (HSDB, 2004): A half-life of 14.4 days on forest foliage. A half-life range of 10.4-26.6 days in foliage and litter in an Oregon coast forest brush habitat. Field studies on glyphosate residue reduction in cowberries, bilberries, reindeer lichen, Cladonia rangifera, and other foliage, produced the following results: At 6-7 days after glyphosate application at 0.75 kg/ha (in July, August, and September), cowberries and bilberries had residue levels of 1.6 and 2.1 ppm, respectively. A 1-2 months, residues levels in these same plants were 0.1-0.3 ppm. At 1 year after a field treatment of 0.25 kg/ha, cowberries and bilberries contained no detectable residues of glyphosate's primary metabolite, aminomethylphosphonic acid (AMPA). At 9 months after application of 0.25, 0.75, and 2.25 kg/ha, springtime glyphosate levels in the reindeer lichen were 2.5, 14, and 45 ppm, respectively. AMPA concentrations were 0.25, 0.84 and 2.1 ppm, respectively. At 13 months after a 0.75 kg/ha treatment, reported glyphosate and AMPA concentrations in one reindeer lichen sample were 6.4 and 0.3 ppm, respectively. Initial foliar residue levels from glyphosate application at 2.0-2.1 kg/ha were 262 and 448 ppm in alder and salmonberry, respectively. At 15 days, residue levels in leaf litter from these same shrubs were 12.5 and 19.2 ppm, respectively. Reported half-lives were 8 days for alder and 9 days for salmonberry.
Reported soil sorption values for glyphosate include the following: H-bonding and ion exchange are considered responsible for glyphosate's strong adsorption potential in many soils. Decreases in pH correlate with increased soil adsorption. A soil's cation exchange capacity (CEC) and the sorbent's surface area reportedly do not affect this relationship (HSDB, 2004). Soil materials that readily adsorb or bind glyphosate include iron and aluminum clays, organic matter, kaolinite, illite, bentonite, charcoal, and muck. Sodium and calcium clays have a lower adsorption potential (HSDB, 2004).
Glyphosate photodegradation on soil surfaces to AMPA, glyphosate's primary degradation product, can be a slow process(Verschueren, 2001). One study reported that a glyphosate level of 25 mg/kg in dry soil did not affect cellulose, starch, protein, or leaf litter degradation, nor did it affect nitrogen fixation after 84 days (Verschueren, 2001).
ABIOTIC DEGRADATION
- Once in the environment, glyphosate readily binds to soil, and to suspended organic matter, and sediment particles in water. In aqueous systems, photodegradation is another means for glyphosate dissipation (HSDB, 2004; Verschueren, 2001; EPA, 2002).
- Glyphosate is strongly adsorbed by many soil types. It has an average half-life of 60 days and is readily degraded by soil microbes. Its mobility in soils is limited by various environmental factors including soil type, pH, temperature, and precipitation. Vaporization from soil and plant surfaces is an insignificant transport pathway, given glyphosate's negligible vapor pressure. Photodegradation on soil surfaces to glyphosate's primary metabolite, aminomethylphosphonic acid (AMPA), can be a slow process (HSDB, 2004; EPA, 2002; Verschueren, 2001; Giesy et al, 2000).
BIODEGRADATION
- The average soil biodegradation half-life for glyphosate is about 60 days. Soil microbes readily biodegrade glyphosate to its primary metabolite, aminomethylphosphonic acid (AMPA), and other inorganic constituents (phosphate and carbon dioxide). Numerous physical and chemical soil factors that affect soil microbial activity also affect glyphosate biodegradation rates (HSDB, 2004; EPA, 2002; Giesy et al, 2000).
- Glyphosate is strongly adsorbed to the upper organic layers in most soils. Biodegradation studies on glyphosate in soil report the following (HSDB, 2004):
Glyphosate decomposition ranges from 10-60% depending on soil and microorganism types. A shake-flask study demonstrated that soil microorganisms can completely biodegrade glyphosate under both aerobic and anaerobic conditions: Under aerobic conditions, 45-55% glyphosate mineralization occurred at 28 days in Ray silt loam, Drummer silty clay loam, and Lintonia sandy loam soils. Under anaerobic conditions in Ray silt loam soil, 37.3% of the glyphosate was released as carbon dioxide (CO2).
At 9 days, 19% of glyphosate biodegraded in Williams silt loam soil (pH 6.4, 1.9% organic matter). At 28 days, 17.4-45.5% of the glyphosate was released as CO2. Carbon dioxide release and biodegradation do not occur in sterilized soil. Addition of phosphate enhances CO2 release. At 30-40 days, glyphosate biodegradation was 50% in three incubated Saskatchewan soils. At 90 days, biodegradation activity in the solvent-extractable and non-extractable fractions from these same three soils was similar at 7-16% and 7-14%, respectively. Glyphosate is thought to be co-metabolized based on its biodegradation pattern.
- Glyphosate degradation studies report that <3% of the initial soil concentration remained at 16 weeks (Verschueren, 2001).
- Glyphosate's primary metabolite from soil biodegradation is aminomethylphosphonic acid (AMPA). AMPA also rapidly biodegrades in soil (HSDB, 2004).
Other microbial biodegradation products for glyphosate include: N-nitrosoglyphosate, ammonia, N,N-dimethylphosphinic acid, N-methylphosphinic acid, aminoacetic acid (glycine), N-methylaminoacetic acid (sarcosine), hydroxymethylphosphonic acid, carbon dioxide, formaldehyde, nitrate, phosphate, and water (Verschueren, 2001). Rhizobiaceae bacteria (Pseudomonas sp. and Arthrobacter atrocyoneus) can use glyphosate as their sole phosphorus source, producing sarcosine, glycine, and formaldehyde as degradation products. The bacterium, Ochrobactrum anthropi, can degrade glyphosate to AMPA (Verschueren, 2001).
BIOACCUMULATION
Glyphosate is not likely to bioaccumulate or bioconcentrate in fish and other aquatic organisms. (HSDB, 2004). In a 55-day study on two Oregon coastal hardwood communities, glyphosate and its primary metabolite, AMPA, were not detected in ten Coho salmon fingerlings (0.05 ppm detection level). Glyphosate was detected in stream water at 3 days and in stream sediment at 55 days (HSDB, 2004).
TERRESTRIAL Glyphosate strongly adsorbs to most soils thus limiting uptake by plant roots. One study showed plants can update glyphosate in quartz sand, but not in sterile soil (HSDB, 2004). Glyphosate concentrations increase in plant foliage that has been sprayed. Concentrations in other plant parts also increase as glyphosate moves downward from the leaves into the stem and root systems (HSDB, 2004).
Glyphosate is unlikely to bioaccumulate in mammals, as it is marginally retained and quickly eliminated. Glyphosate reportedly does not bioaccumulate in higher trophic level organisms (herbivores, omnivores, carnivores) (HSDB, 2004).
OTHER Glyphosate does not bioaccumulate in higher trophic level organisms (herbivores, omnivores, carnivores) (HSDB, 2004)
Crustacean (Procambarus simulans): 9 (BCF, edible portions) and 8 (BCF,whole body) -- 28 D at 3000 mcg/L (Verschueren, 2001). Fish: 0.2-0.3 -- 10-14D (HSDB, 2004) Fish (Ictalurus punctatus) : 0.18 (BCF, whole body) -- 14D at < 10,000 mcg/L; 0.26 (BCF, whole body) -- 10D at < 1000 mcg/L (Verschueren, 2001) Fish (Micropterus salmoides): 0.03-0.04 (BCF, whole body) -- 14 D at <10,000 mcg/L (Verschueren, 2001) Mollusc (Rangia cuneata): 9.6 (BCF, edible portion) -- 35D at 500 mcg/L; 4.8 (BCF, edible portion) -- 28D at 3000 mcg/L (Verschueren, 2001)
ENVIRONMENTAL TOXICITY
Technical grade glyphosate acid (CAS 1071-83-6) is reportedly more toxic than the isopropylamine (IPA) salt form (CAS 38641-94-0) for some aquatic organisms due to the higher acidity (lower test media pH) caused by acid versus the salt form (Tsui & Chu, 2003). Glyphosate is a weak acid. As a 1% aqueous solution, its pH is approximately 2 (Tsui & Chu, 2003; Krieger, 2001). Environmental factors such as temperature, organic matter content, and pH may substantially affect the acute or chronic toxicity of glyphosate, the IPA salt form, and the various glyphosate formulations (HSDB, 2004; Tsui & Chu, 2003). At higher temperatures, glyphosate was twice as toxic to rainbow trout (17 vs 7 degrees C) and bluegills (27 vs 17 degrees C) (HSDB, 2004). At increase in pH from 6.5 to 7.5-9.5, increased glyphosate toxicity two to four times in bluegills and rainbow trout (HSDB, 2004).
Glyphosate formulations containing the surfactant polyoxyethyleneamine (POEA) tend to be more toxic to amphibians and aquatic organisms than formulations containing no added surfactants or technical grade glyphosate alone (Howe et al, 2004; Perkins et al, 2000). A recent study using amphibian (Xenopus laevis) embryos reported an LC50 of 6.8 mg/L for the surfactant POEA itself. This was compared to an LC50 of 7,297 mg-(acid equivalent)/L for a common glyphosate herbicide containing no surfactants, and an LC50 of 9.3 mg-(acid equivalent)/L for a common glyphosate herbicide containing POEA (Perkins et al, 2000).
Aquatic Organisms ALGAE EC50 - BLUE-GREEN ALGAE (Anabaena flos-aquae): 15 mg/L for 7D -- growth inhibition (Verschueren, 2001) EC50 - GREEN ALGAE (Selenastrum capricornutum): 0.01 mg/L -- oxygen evolution inhibition; 0.0038 mg/L -- growth inhibition; 35, 44, 70 mg/L -- photosynthesis inhibition; <25, <100 mg/L -- nitrogen fixation inhibition (Verschueren, 2001) EC50 - GREEN ALGAE (Selenastrum capricornutum): 1.1 mg/L for 72H -- nitrogen fixation inhibition (Verschueren, 2001) EC50 - GREEN ALGAE (Selenastrum capricornutum): 13.8 and 485 mg/L for 7D -- growth inhibition (Verschueren, 2001) EC50 - DIATOM (Skeletonema costatum): 0.64 mg/L for 7D; 1.3 mg/L for 96H -- growth inhibition (Verschueren, 2001) EC50 - DIATOM (Navicula pelliculosa): 42 mg/L for 7D -- growth inhibition (Verschueren, 2001) EC100 - GREEN ALGAE (Selenastrum capricornutum): 3.2 mg/L for 72H -- nitrogen fixation inhibition (Verschueren, 2001) IC50 - DIATOM (Skeletonema costatum): 2.27 mg (acid equivalent)/L for 96H, glyphosate acid, (95% CI=0.82-11.1) -- growth inhibition (Tsui & Chu, 2003) IC50 - GREEN ALGAE (Selenastrum capricornutum): -- 24.7 mg (acid equivalent)/L for 96H, glyphosate acid, (95% CI=22.8-26.7) -- growth inhibition (Tsui & Chu, 2003) NOEC - GREEN ALGAE (Selenastrum capricornutum): 45 mg/L for 7D -- growth inhibition (Verschueren, 2001)
AQUATIC PLANTS EC50 - DUCKWEED (Lemna gibba): 25.5 mg/L for 14 D -- growth inhibition (Verschueren, 2001) NOEC - DUCKWEED (Lemna gibba): 16.6 mg/L for 14 D -- growth inhibition (Verschueren, 2001)
AMPHIBIANS LC5 - AFRICAN CLAWED FROG (Xenopus laevis) embryo: 5515.5 mg (acid equivalent)/L [acid equivalent basis (AE) in mg/L] for Rodeo(R) and 7.7 mg (acid equivalent)/L for Roundup(R) at 96H -- FETAX bioassay (Perkins et al, 2000) LC10 - AFRICAN CLAWED FROG (Xenopus laevis) embryo: 5867.2 mg/L [acid equivalent basis (AE) in mg/L] for Rodeo(R) and 8.0 mg (acid equivalent)/L for Roundup(R) at 96H -- FETAX bioassay (Perkins et al, 2000) LC50 - AFRICAN CLAWED FROG (Xenopus laevis) embryo: 7296.8 mg/L [acid equivalent basis (AE) in mg/L] for Rodeo(R) and 9.3 mg (acid equivalent)/L for Roundup(R) at 96H -- FETAX bioassay (Perkins et al, 2000) LC50 - GREEN FROG (Rana clamitans), tadpoles (stage 25): >39.9 mg/L [equivalent to >17.9 mg (glyphosate acid)/L] for 24H and 96H, technical grade glyphosate (Howe et al, 2004)
CRUSTACEANS EC50 - WATER FLEA (Daphnia magna): 780 mg/L for 48H (Verschueren, 2001) EC50 - GRASS SHRIMP (Palaemonetes vulgaris): 281 mg/L for 96H (Verschueren, 2001) LD50 - CLADOCERAN (Ceriodaphnia dubia): 147 mg (acid equivalent)/L for 48H, glyphosate acid, (95% CI=141-153) (Tsui & Chu, 2003) LD50 - COPEPOD (Acartia tonsa): 35.3 mg (acid equivalent)/L for 48H, glyphosate acid, (95% CI=30.9-40.3) (Tsui & Chu, 2003) LC50 - CRAWFISH: 21,632 mg/L for 96H (Verschueren, 2001) LC50 - FIDDLER CRAB (Uca pugilator): 934 mg/L for 96H (Verschueren, 2001) LC50 - RED SWAMP CRAWFISH (Procambus clarki): 47 mg/L for 4D (Verschueren, 2001) LC50 - SHRIMP (Mysidopsis bahia): >1,000 mg/L for 96H (Verschueren, 2001) MATC - WATER FLEA (Daphnia magna): 50-96 mg/L for 21D (Verschueren, 2001) NOEC - FIDDLER CRAB (Uca pugilator): 650 mg/L for 96H (Verschueren, 2001) NOEC - WATER FLEA (Daphnia magna): 560 mg/L for 48H; 50,100 mg/L for 21D(Verschueren, 2001)
FISH LC0 - HARLEQUINFISH (Rasbora hetermorpha): 168 mg/L for 96H (Verschueren, 2001) LC50 - BLUEGILL SUNFISH (Lepomis macrochirus): 120 mg/L for 96H (Verschueren, 2001) LC50 - BLUEGILL SUNFISH (Lepomis macrochirus): 13 mg/L for 96H (Verschueren, 2001) LC50 - BLUEGILL SUNFISH (Lepomis macrochirus), wt=0.9g: 135 mg/L for 96H (95% CI=113-162), technical grade -- static bioassay, test conditions: no aeration, pH 7.2-7.5, hardness 40-50 mg/L as CaCO3, alkalinity 30-35 mg/L, 22 degrees C (HSDB, 2004) LC50 - CHANNEL CATFISH (Ictalurus punctatus): 14.5 mg/L for 96H (Verschueren, 2001) LC50 - CHANNEL CATFISH (Ictalurus punctatus), wt=2.2g: 130 mg/L for 96H (95% CI=108-156), technical grade -- static bioassay, test conditions: no aeration, pH 7.2-7.5, hardness 40-50 mg/L as CaCO3, alkalinity 30-35 mg/L, 22 degrees C (HSDB, 2004) LC50 - FATHEAD MINNOW (Pimephales promelas), wt=0.6g: 97 mg/L for 96H (95% CI=79-120), technical grade -- static bioassay, test conditions: no aeration, pH 7.2-7.5, hardness 40-50 mg/L as CaCO3, alkalinity 30-35 mg/L, 20 degrees C (HSDB, 2004) LC50 - FLAGFISH: 30 mg/L for 8D (Verschueren, 2001) LC50 - RAINBOW TROUT (Salmo gairdneri): 86 mg/L for 96H (Verschueren, 2001) LC50 - RAINBOW TROUT (Salmo gairdneri), wt=0.8g: 130 mg/L for 96H (95% CI=108-156), technical grade -- static bioassay, test conditions: no aeration, pH 7.2-7.5, hardness 40-50 mg/L as CaCO3, alkalinity 30-35 mg/L (HSDB, 2004) MATC -- FATHEAD MINNOW (Pimephales promelas): >25.7 mg/L for 255D (Verschueren, 2001) NOEC - BLUEGILL SUNFISH (Lepomis macrochirus): 100 mg/L for 96H (Verschueren, 2001) NOEC - RAINBOW TROUT (Salmo gairdneri): 42 mg/L for 96H (Verschueren, 2001)
INSECTS EC50 - MIDGE (Chironomus riparius), larvae: 5,600 mg/L for 48H (Verschueren, 2001) LC50 - MALARIA MOSQUITO (Anopheles quadrimaculatus): 673 mg/L for 24H (Verschueren, 2001)
MICROORGANISMS EC20 - BACTERIA (Photobacterium phosphoreum): 0.75 mg/L for 5 min (Biotox bioassay)(Verschueren, 2001) EC50 - BACTERIA (Photobacterium phosphoreum): 2.2 mg/L for 5 min (Biotox bioassay); 7.7 mg/L for 5 min (Microtox bioassay) (Verschueren, 2001) IC50 - BACTERIA (Vibrio fischeri): 17.5 mg (acid equivalent)/L for 15 min, glyphosate acid, (95% CI=15.8-19.5) -- median growth inhibition , Microtox bioassay (Tsui & Chu, 2003) IC50 - PROTOZOA (Euplotes vannus): 10.1 (acid equivalent)/L for 48H, glyphosate acid, (95% CI=6.47-14.5) -- median growth inhibition (Tsui & Chu, 2003) IC50 - PROTOZOA (Tetrahymena pyriformis): 648 mg (acid equivalent)/L for 40H, glyphosate acid, (95% CI=430-1280) -- median growth inhibition (Tsui & Chu, 2003) NOEC - SOIL BACTERIA: >25 mg/kg for 84D(Verschueren, 2001)
MOLLUSCS
Terrestrial Organisms BIRDS LD50 - (ORAL) BOBWHITE QUAIL: >3850 mg/kg, technical grade (HSDB, 2004) LD50 - (DIET) QUAIL: >4640 ppm for 8 days, technical grade (HSDB, 2004)
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
DESCRIPTION/PHYSICAL STATE
- Glyphosate exists as colorless to white crystals (Budavari, 2001; Verschueren, 2001; Tomlin, 2000).
VAPOR PRESSURE
- <10(-7) hPa (at 45 degrees C) (Verschueren, 2001)
- 1.31 x 10(-2) mPa (at 25 degrees C) (Tomlin, 2000)
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
DENSITY
- TEMPERATURE AND/OR PRESSURE NOT LISTED
FREEZING/MELTING POINT
189.5 degrees C (Verschueren, 2001) 189.5 +/- 0.5 degrees C (Tomlin, 2000)
SOLUBILITY
10,000 mg/L (at 25 degrees C) (Verschueren, 2001) 11.6 g/L (at 25 degrees C) (Tomlin, 2000) 12 g/L (at 25 degrees C) (Budavari, 2001)
insoluble in most common organic solvents, such as acetone, ethanol, and xylene (Budavari, 2001; Tomlin, 2000)
OCTANOL/WATER PARTITION COEFFICIENT
- log P = 0.001 - 0.002 (measured) (Verschueren, 2001)
- log P = <-3.2 (at pH 2 - 5 and 20 degrees C) (Tomlin, 2000)
HENRY'S CONSTANT
- <2.1 x 10(-7) Pa m(3)/mol (Tomlin, 2000)
OTHER/PHYSICAL
- DECOMPOSITION TEMPERATURE
decomposes at >200 degrees C (Tomlin, 2000) 230 degrees C (Budavari, 2001; Lide, 2003)
pKa = 5.77 +/- 0.03 (Tomlin, 2000) pKa = 2.18 +/- 0.02 (at 20 +/- 2 degrees C) (Tomlin, 2000)
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