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PYRIDINE HERBICIDES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Pyridine herbicides include aminopyralid, clopyralid, dithiopyr, fluroxypyr, triclopyr, thiazopyr, fluroxypyr, and thiazopyr. They are used primarily to limit the growth of broad leaf weeds. For management of PICLORAM toxicity, please see the separate PICLORAM document.

Specific Substances

    A) AMINOPYRALID
    1) 4-amino-3,6-dichloropyridine-2-carboxylic acid
    2) CAS 150114-71-9
    CLOPYRALID
    1) Acide 3,6-dcp
    2) Acide 3,6-dichloropicolinique (French)
    3) Benzalox
    4) Campaign
    5) Cirtoxin
    6) Crusader S
    7) Cyronal
    8) 3,6-DCP
    9) 3,6-Dichloropicolinic acid
    10) 3,6-Dichloro-2-pyridinecarboxylic acid
    11) Dowco 290
    12) Escort
    13) Format
    14) Kyselina 3,6-dichlorpikolinova (Czech)
    15) Lontrel
    16) Lontrel 3
    17) Lontrel SF 100
    18) Matrigon
    19) Picolinic acid, 3,6-dichloro-
    20) 2-Pyridinecarboxylic acid, 3,6-dichloro- (9CI)
    21) Reclaim
    22) Shield
    23) XRM 3972
    24) CAS 1702-17-6
    DITHIOPYR
    1) MON 15100
    2) MON 7200
    3) 3,5-Pyridinedicarbothioic acid,2-(difluoromethyl)-4-(2-methylpropyl)-6-(trifluoromethyl)-,S,S-dimethyl ester
    4) CAS 97886-45-8
    FLUROXYPYR
    1) Acetic acid, ((4-amino-3,5-dichloro-6-fluoro-2-pyridinyl)oxy)-
    2) ((4-Amino-3,5-dichloro-6-fluoro-2-pyridinyl)oxy)acetic acid
    3) 4-Amino-3,5-dichloro-6-fluoro-2-pyridyloxyacetic acid
    4) Advance
    5) FF4014
    6) Starane
    7) CAS 69377-81-7
    PYRICLOR
    1) Daxtron
    2) 4-Pyridinol, 2,3,5-trichloro-
    3) 2,3,5-Trichloro-4-hydroxypyridine
    4) 2,3,5-Trichloro-4-pyridinol
    5) CAS 1970-40-7
    THIAZOPYR
    1) Mandate
    2) Methyl-2-difluoromethyl-5-(4,5-dihydro-1,3-thiazol-2-yl)-4-isobutyl-6-trifluorom ethylnicotinate
    3) Methyl-2-difluoromethyl-5-(4,5-dihydro-2-thiazolyl)-4-(2-methylpropyl)-6-(trifluoromethyl)-3-pyridinecarboxylate
    4) MON 13200
    5) 3-Pyridinecarboxylic acid,2-(difluoromethyl)-5-(4,5-dihydro-2-thiazolyl)-4-(2-methylpropyl)-6-(trifluoromethyl)-, methyl ester
    6) Thiazophyr
    7) Visor
    8) CAS 117718-60-2
    TRICLOPYR
    1) Acetic acid, (3,5,6-trichloro-2-pyridyloxy)-
    2) Crossbow
    3) Dowco 233
    4) Garlon
    5) Grazon ET
    6) Redeem
    7) 3,5,6-Trichloro-2-pyridyloxyacetic acid
    8) Turflon
    9) CAS 55335-06-3
    10) HERBICIDES, PYRIDINE

Available Forms Sources

    A) FORMS
    1) FLUROXYPYR: Fluroxypyr may be formulated as an emulsified concentrate. It can be applied as fluroxypyr-meptyl (Meister, 2012).
    2) THIAZOPYR: Thiazopyr may be formulated as an emulsifiable concentrate, as granules, or a wettable powder (HSDB - Hazardous Substances Data Bank, 2002).
    3) TRICLOPYR: Triclopyr may be formulated as an emulsifiable concentrate, granular flakes, or a miscible liquid (Meister, 2012).
    B) SOURCES
    1) CLOPYRALID: Occupational exposure to clopyralid may be by inhalation or dermal exposure at workplaces where clopyralid is produced or used. The general population may be exposed through inhalation of ambient air or through ingestion of drinking water (HSDB - Hazardous Substances Data Bank, 2013).
    2) FLUROXYPYR: Occupational exposure to fluroxypyr may occur by dermal contact or through inhalation in the workplace where it is produced or used. The general population may be exposed from inhalation or dermal contact with this compound. Exposure may also occur when using lawn-care products containing fluroxypyr or following applications at parks, golf courses, or other grassy areas (HSDB - Hazardous Substances Data Bank, 2011).
    C) USES
    1) CLOPYRALID: Clopyralid is used as a herbicide for post-emergence control of many annual and perennial broad leaved weeds of the families Compositae, Leguminosae, Polygonaceae, and Umbelliferae. It is particularly good for providing control of perennial sow-thistle, creeping thistle (Cirsium arvense), coltsfoot, mayweeds, and Polygonum species (Meister, 2012). It is also used for control in barley, canola, corn, mint, oats, wheat, sugarbeets, spinach, turnips Christmas tree plantations, fallow land, grasses grown for seed, non-crop land, and permanent grass pastures (HSDB - Hazardous Substances Data Bank, 2013).
    2) DITHIOPYR: Dithiopyr is used as a herbicide for selective control of certain annual broadleaf weeds (Meister, 2012).
    3) FLUROXYPYR: Fluroxypyr is an herbicide used to control weeds in cereals, fallow land, and on farm non-crop land (Meister, 2012). It is registered with the United States Environmental Protection Agency (EPA) for use on pasture and rangeland; crops including sweet corn, field corn, wheat, barley, oats, millet, sorghum, onions, apple and pear orchards; pine plantations, fallow cropland, industrial sites, rights-of-way-electrical power lines, communication lines, pipelines, roadsides, railroads, residential lawns; recreational sites including golf courses, parks, and sports fields (HSDB - Hazardous Substances Data Bank, 2011).
    4) THIAZOPYR: Thiazopyr is used as a herbicide for pre-emergent weeds, annual grasses and certain broadleaf weeds. It is also used for pre-emergent control of annual grasses and some broad-leaf weeds in tree fruits, vines, citrus, sugar cane, pineapples, alfalfa, and forestry. It is generally applied at 0.1 to 0.56 kg/ha (HSDB - Hazardous Substances Data Bank, 2002).
    5) TRICLOPYR: Triclopyr is an herbicide used to control woody plants and broadleaf weeds on industrial sites, rights-of-way, turf, permanent grass pastures, rangeland, and non-irrigation ditch banks (Meister, 2012).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Pyridine herbicides are used to control unwanted plant growth. Frequently, they are used to limit the growth of broad leaf weeds around power lines and on residential lawns, golf courses, parks, and crops. Herbicides in this group include: aminopyralid, clopyralid, dithiopyr, fluroxypyr, thiazopyr, triclopyr, and picloram. For management of PICLORAM toxicity, please see the separate PICLORAM document.
    B) TOXICOLOGY: The mechanism of action is by mimicking auxin, a natural growth inhibiting hormone in plants. Some dermal absorption does occur with regular use, resulting in detectable urine concentrations. This does not correlate with clinical symptoms.
    C) EPIDEMIOLOGY: Widely used in the world but human data on acute poisoning following exposure are limited.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Pyridine herbicides are considered low toxicity herbicides. There is limited human poisoning data. Healthy subjects have received 0.5 mg/kg of triclopyr safely. Triclopyr is irritating to eyes.
    2) SEVERE TOXICITY: Clopyralid is a severe eye irritant. A single case report exists of hypotension, metabolic acidosis, coma and cardiovascular impairment after intentional ingestion of triclopyr.
    0.2.20) REPRODUCTIVE
    A) Clopyralid produced developmental abnormalities of the musculoskeletal system in the offspring of rats. Triclopyr esters produced minor skeletal malformations in the offspring of rats.

Laboratory Monitoring

    A) Plasma concentrations of these herbicides are not readily available or clinically useful in guiding therapy.
    B) Monitor vital signs and mental status.
    C) Monitor serum electrolytes in patients with severe gastrointestinal symptoms after large or deliberate ingestions.
    D) Obtain an ECG and institute continuous cardiac monitoring after large or deliberate ingestions.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Most cases of exposure to pyridine herbicides will not have significant symptoms. Treatment should be symptomatic and supportive.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment should be symptomatic and supportive. Administer IV fluids for hypotension; add vasopressors if hypotension persists. A single case report exists of hypotension, metabolic acidosis, coma and cardiovascular impairment after intentional ingestion of triclopyr.
    C) DECONTAMINATION
    1) PREHOSPITAL: Wash exposed skin with soap and water and remove contaminated clothing. Irrigate exposed eyes. Gastrointestinal decontamination is not recommended unless another more toxic agent is involved.
    2) HOSPITAL: Remove contaminated clothing and wash exposed skin with soap and water. Irrigate exposed eyes with water or 0.9% saline. Gastrointestinal decontamination is not recommended after ingestion unless a more toxic agent is also involved.
    D) AIRWAY MANAGEMENT
    1) Loss of airway reflexes or respiratory inhibition is not expected following isolated pyridine ingestion. Airway management may be necessary in patients who develop CNS depression after large ingestions.
    E) ANTIDOTE
    1) No specific antidote.
    F) ENHANCED ELIMINATION
    1) No data suggest use of enhanced elimination.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with no or minimal symptoms after inadvertent exposure may be observed at home.
    2) OBSERVATION CRITERIA: Symptomatic patients and those with deliberate exposure should be referred to a healthcare facility. Observe symptomatic patients until symptoms are resolved.
    3) ADMISSION CRITERIA: Patients with acidosis, coma, evidence of cardiovascular toxicity, or severe gastrointestinal symptoms should be admitted to the hospital.
    4) CONSULT CRITERIA: Consult a Poison Center or medical toxicologist for assistance in managing patients with severe toxicity or for whom diagnosis is unclear.
    H) PITFALLS
    1) Pitfalls include not evaluating for other coingestants such as solvents or surfactants, which may be ingredients included with the herbicide.
    I) TOXICOKINETICS
    1) Some dermal absorption does occur with regular use, resulting in detectable urine concentrations. This does not correlate with clinical symptoms.
    J) DIFFERENTIAL DIAGNOSIS
    1) Consider poisoning with other non-pyridine herbicides.

Range Of Toxicity

    A) TOXICITY: A toxic dose has not been well established. Severity of intoxication should be based on clinical findings. These agents appear to have low systemic toxicity. The World Health Organization (WHO) has classified clopyralid, diflufenican, dithiopyr, florasulam, and fluroxypyr as Class U (unlikely to present acute hazard in normal use). Triclopyr is classified as Class III (slightly hazardous). Healthy volunteers have received 0.5 mg/kg of triclopyr safely. A 57-year-old man survived intentional ingestion of 300 mL of triclopyr (estimated ingested amount of triclopyr: 1500 mg/kg; 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, 65.5% water). Three patients survived after ingesting triclopyr 70% (doses: 5 mL, 40 mL, and 300 mL).

Clinical Effects

Summary Of Exposure

    A) USES: Pyridine herbicides are used to control unwanted plant growth. Frequently, they are used to limit the growth of broad leaf weeds around power lines and on residential lawns, golf courses, parks, and crops. Herbicides in this group include: aminopyralid, clopyralid, dithiopyr, fluroxypyr, thiazopyr, triclopyr, and picloram. For management of PICLORAM toxicity, please see the separate PICLORAM document.
    B) TOXICOLOGY: The mechanism of action is by mimicking auxin, a natural growth inhibiting hormone in plants. Some dermal absorption does occur with regular use, resulting in detectable urine concentrations. This does not correlate with clinical symptoms.
    C) EPIDEMIOLOGY: Widely used in the world but human data on acute poisoning following exposure are limited.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Pyridine herbicides are considered low toxicity herbicides. There is limited human poisoning data. Healthy subjects have received 0.5 mg/kg of triclopyr safely. Triclopyr is irritating to eyes.
    2) SEVERE TOXICITY: Clopyralid is a severe eye irritant. A single case report exists of hypotension, metabolic acidosis, coma and cardiovascular impairment after intentional ingestion of triclopyr.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) CLOPYRALID: Clopyralid is a severe eye irritant (HSDB - Hazardous Substances Data Bank, 2013)
    2) TRICLOPYR: Based on a review of pesticide poisoning incident data, 12 individuals experienced eye irritation when they handled or were exposed by drift to triclopyr. Based on the evidence, these cases were not considered severe (U.S. Environmental Protection Agency (EPA), 1998).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) TRICLOPYR: A 57-year-old man with a history of hypertension and colon cancer was found by his wife unconscious after intentionally ingesting approximately 300 mL of triclopyr herbicide composed of 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, and 65.5% water. He presented to the emergency department 2.5 hours post-ingestion with agitation, confusion, cyanosis, and hypotension (BP 90/60 mmHg). Following gastric decontamination, he was intubated and transferred to a specialty critical care facility. Laboratory results revealed metabolic acidosis. Sinus tachycardia and a prolonged QTc interval of 533 ms were observed on an ECG. An echocardiogram showed an ejection fraction of 42% with global hypokinesia. Laboratory analysis showed increased serum phosphokinase of greater than 3000 international units (IU)/L (normal range; less than 244 IU/L); serum troponin T of 0.928 nanograms (ng)/mL (normal range; less than 0.1 ng/mL); CK-MB of 73 ng/mL (normal range; less than 5 ng/mL). Peak enzyme concentrations were recorded 1 to 2 days after ingestion. He was admitted to the intensive care unit where he received supportive treatment. Responsiveness returned 10.5 hours after ingestion. At 57 hours post-ingestion, he had recovered fully and was extubated. Ejection fraction improved to 62% by day 13 of his hospitalization. He was discharged to a psychiatric unit on day 14 (Kyong et al, 2010).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) TRICLOPYR: A 57-year-old man with a history of hypertension and colon cancer was found by his wife unconscious after intentionally ingesting approximately 300 mL of triclopyr herbicide composed of 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, and 65.5% water. He presented to the emergency department 2.5 hours post-ingestion with agitation, confusion, cyanosis, and hypotension (BP 90/60 mmHg). Following gastric decontamination, he was intubated and transferred to a specialty critical care facility. Laboratory results revealed metabolic acidosis and elevated cardiac enzymes. Sinus tachycardia and a prolonged QTc interval of 533 ms were observed on ECG. An echocardiogram showed an ejection fraction of 42% with global hypokinesia. He was admitted to the intensive care unit where he received supportive treatment. Responsiveness returned 10.5 hours after ingestion. At 57 hours post-ingestion, he had recovered fully and was extubated. He was discharged to a psychiatric unit on day 14 (Kyong et al, 2010).

Respiratory

    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY FINDING
    a) AMINOPYRALID: In animal studies, rats were exposed to nose-only inhalation of a dust aerosol containing aminopyralid (purity: 94.5%) at 5.5 mg/L. Gasping was observed immediately after exposure in one male rat. During the first week after exposure, dried red material was observed around the nose of one female rat (Hazardous Substances Data Bank (HSDB), 2012).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) COMA
    1) WITH POISONING/EXPOSURE
    a) TRICLOPYR: A 57-year-old man with a history of hypertension and colon cancer was found by his wife unconscious after intentionally ingesting approximately 300 mL of triclopyr herbicide composed of 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, and 65.5% water. He presented to the emergency department 2.5 hours post-ingestion with agitation, confusion, cyanosis, and hypotension (BP 90/60 mmHg). Following gastric decontamination, he was intubated and transferred to a specialty critical care facility. Laboratory results revealed metabolic acidosis and elevated cardiac enzymes. Sinus tachycardia and a prolonged QTc interval of 533 ms were observed on ECG. An echocardiogram showed an ejection fraction of 42% with global hypokinesia. He was admitted to the intensive care unit where he received supportive treatment. Responsiveness returned 10.5 hours after ingestion. At 57 hours post-ingestion, he had recovered fully and was extubated. He was discharged to a psychiatric unit on day 14 (Kyong et al, 2010).

Hepatic

    3.9.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) LIVER DAMAGE
    a) DITHIOPYR: Changes in liver weight, hepatitis, hepatocellular necrosis, and cholestatic jaundice have been observed in rodents and dogs (RTECS, 2003).
    b) THIAZOPYR: Carcinogenicity studies in mice and rats revealed increased liver weight; periportal hepatocellular vacuolation; hepatocellular hypertrophy; significant increase in microscopic lesions in the liver; and slight increases in ALP, SGOT and SGPT (EPA, 1997).

Genitourinary

    3.10.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) UROGENITAL FINDING
    a) THIAZOPYR: Increased kidney weight and kidney nephropathy were noted in a carcinogenicity study in mice (EPA, 1997).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) TRICLOPYR: A 57-year-old man with a history of hypertension and colon cancer was found by his wife unconscious after intentionally ingesting approximately 300 mL of triclopyr herbicide composed of 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, and 65.5% water. He presented to the emergency department 2.5 hours post-ingestion with agitation, confusion, cyanosis, and hypotension (BP 90/60 mmHg). Following gastric decontamination, he was intubated and transferred to a specialty critical care facility. Laboratory results revealed metabolic acidosis (pH 7.3; PCO2 30.7 mmHg; PO2 144.8 mmHg; HCO3 15 mmol/L with 100% oxygenation) and elevated cardiac enzymes. Sinus tachycardia and a prolonged QTc interval of 533 ms were observed on ECG. An echocardiogram showed an ejection fraction of 42% with global hypokinesia. He was admitted to the intensive care unit where he received supportive treatment. Responsiveness returned 10.5 hours after ingestion. At 57 hours post-ingestion, he had recovered fully and was extubated. He was discharged to a psychiatric unit on day 14 (Kyong et al, 2010).

Hematologic

    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HEMATOLOGY FINDING
    a) DITHIOPYR: Changes in serum composition (eg; TP, bilirubin, cholesterol) have been noted in dogs (RTECS, 2003).
    b) CLOPYRALID: Northern bobwhite (Colinus virginianus) chicks exposed to clopyralid as embryos did not develop immunological deficiencies as measured by response to PHA and sheep RBC challenge (Dabbert et al, 1996).

Dermatologic

    3.14.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SKIN IRRITATION
    a) CLOPYRALID: Clopyralid is a mild skin irritant with prolonged or repeated contact (HSDB - Hazardous Substances Data Bank, 2013).
    b) DITHIOPYR: The emulsified concentrate (12.7%) is labeled as a skin irritant and is a sensitizer in the Buehler assay (Krieger, 2001).
    c) THIAZOPYR: Thiazopyr is moderately irritating to the skin. It is not a sensitizer (EPA, 1997).

Endocrine

    3.16.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ENDOCRINE FINDING
    a) CLOPYRALID: Enlarged adrenal cortical cells were observed in dogs exposed to clopyralid (HSDB - Hazardous Substances Data Bank, 2013).
    b) THIAZOPYR: Increased thyroid weight and a significant increase in microscopic lesions in the thyroid (hypertrophy and hyperplasia) were observed in a 2 year carcinogenicity study in rats (EPA, 1997).

Reproductive

    3.20.1) SUMMARY
    A) Clopyralid produced developmental abnormalities of the musculoskeletal system in the offspring of rats. Triclopyr esters produced minor skeletal malformations in the offspring of rats.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) MUSCULOSKELETAL FINDING
    a) Clopyralid: Clopyralid produced developmental abnormalities of the musculoskeletal system in the offspring of rats given 150 mg/kg orally on day 6 through 15 of gestation (RTECS, 2003).
    b) A higher incidence of a fourteenth thoracolumbar rib was seen in the offspring of rats given 300 mg/kg of triclopyr butoxyethyl ester (equivalent to 216 mg/kg triclopyr) on day 6 through 15 of gestation. Offspring of rats given up to 300 mg/kg of triclopyr triethylamine salt (equivalent to 216 mg/kg triclopyr) did not have a higher incidence of malformations compared to controls (Carney et al, 2007).
    2) LACK OF EFFECT
    a) Clopyralid: In another study, rats were given clopyralid at doses of 0, 15, 75 or 250 mg/kg/day on days 6 through 15 of gestation and rabbits were given 0, 110, or 250 mg/kg on days 6 through 18 of gestation. No teratogenic effects were seen in either the rats or rabbits (Hayes et al, 1984).
    b) Triclopyr: Offspring of rats given doses of 50, 100, and 200 mg/kg/day on days 6 to 15 of gestation had no birth defects; mild fetotoxicity was noted. No teratogenic effects were observed in the offspring of rabbits given doses of 10 and 25 mg/kg/day on days 6 to 18 of gestation (EXTOXNET, 1996).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Triclopyr: No reproductive toxicity was observed in rats and rabbits given triclopyr during pregnancy (EXTOXNET, 1996).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS55335-06-3 (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):
    1) Not Listed
    B) IARC Carcinogenicity Ratings for CAS97886-45-8 (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):
    1) Not Listed
    C) IARC Carcinogenicity Ratings for CAS1970-40-7 (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):
    1) Not Listed
    D) IARC Carcinogenicity Ratings for CAS117718-60-2 (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):
    1) Not Listed
    E) IARC Carcinogenicity Ratings for CAS69377-81-7 (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):
    1) Not Listed
    F) IARC Carcinogenicity Ratings for CAS1702-17-6 (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):
    1) Not Listed
    3.21.4) ANIMAL STUDIES
    A) ENDOCRINE FINDING
    1) Thiazopyr: Thiazopyr is considered neoplastic by RTECS criteria and has produced thyroid tumors in rodents (RTECS, 2003; Hurley et al, 1998).
    a) Thiazopyr chronically administered to male Sprague-Dawley rats at 1000 ppm and 3000 ppm produced thyroid follicular cell tumors. Female rats were not affected. This effect was thought to be due to sustained increases on TSH which caused follicular cell hypertrophy and hyperplasia which subsequently led to malignancy. No effect was observed at doses of 100 ppm. Sustained increases in TSH are not thought to lead to tumor production in humans (Hotz et al, 1997).
    b) A subsequent review noted that thyroid metabolism is fundamentally different between rats and humans. Based on these differences, thiazopyr was highly unlikely to produce thyroid tumors in humans (Dellarco et al, 2006).
    B) LACK OF EFFECT
    1) Triclopyr: No carcinogenic response was noted in rats and mice fed oral doses of triclopyr at 3 to 30 mg/kg/day for 2 years (EXTOXNET, 1996).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Plasma concentrations of these herbicides are not readily available or clinically useful in guiding therapy.
    B) Monitor vital signs and mental status.
    C) Monitor serum electrolytes in patients with severe gastrointestinal symptoms after large or deliberate ingestions.
    D) Obtain an ECG and institute continuous cardiac monitoring after large or deliberate ingestions.
    4.1.2) SERUM/BLOOD
    A) Plasma concentrations of these herbicides are not readily available or clinically useful in guiding therapy.
    B) Monitor serum electrolytes in patients with severe gastrointestinal symptoms after large or deliberate ingestions.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Monitor vital signs and mental status.
    b) Obtain an ECG and institute continuous cardiac monitoring after large or deliberate ingestions.

Methods

    A) CLOPYRALID: Residues and clopyralid can be analyzed by gas liquid chromatography (HSDB - Hazardous Substances Data Bank, 2013).
    B) FLUROXYPYR: Residues of fluroxypyr-meptyl and fluroxypyr can be determined by high performance liquid chromatography (HSDB - Hazardous Substances Data Bank, 2011).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with acidosis, coma, evidence of cardiovascular toxicity, or severe gastrointestinal symptoms should be admitted to the hospital.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with no or minimal symptoms after inadvertent exposure may be observed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a Poison Center or medical toxicologist for assistance in managing patients with severe toxicity or for whom diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Symptomatic patients and those with deliberate exposure should be referred to a healthcare facility. Observe symptomatic patients until symptoms are resolved.

Monitoring

    A) Plasma concentrations of these herbicides are not readily available or clinically useful in guiding therapy.
    B) Monitor vital signs and mental status.
    C) Monitor serum electrolytes in patients with severe gastrointestinal symptoms after large or deliberate ingestions.
    D) Obtain an ECG and institute continuous cardiac monitoring after large or deliberate ingestions.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Exposure to pyridine herbicides is generally NOT expected to result in significant toxicity. Remove contaminated clothing and wash exposed areas with soap and water. Irrigate exposed eyes thoroughly. Gastrointestinal decontamination is not recommended unless a more toxic agent is involved. Following an inhalational exposure, move patient to fresh air.
    6.5.2) PREVENTION OF ABSORPTION
    A) ACTIVATED CHARCOAL
    1) Gastrointestinal decontamination is not recommended after ingestion unless a more toxic agent is also involved.
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Most cases of exposure to pyridine herbicides will not have significant symptoms. Treatment should be symptomatic and supportive.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment should be symptomatic and supportive. Administer IV fluids for hypotension; add vasopressors if hypotension persists. A single case report exists of hypotension, metabolic acidosis, coma and cardiovascular impairment after intentional ingestion of triclopyr.
    B) MONITORING OF PATIENT
    1) Plasma concentrations of these herbicides are not readily available or clinically useful in guiding therapy.
    2) Monitor vital signs and mental status.
    3) Monitor serum electrolytes in patients with severe gastrointestinal symptoms after large or deliberate ingestions.
    4) Obtain an ECG and institute continuous cardiac monitoring after large or deliberate ingestions.
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) PROLONGED QT INTERVAL
    1) Prolongation of the QT interval has been reported in a patient exposed to triclopyr herbicide (Kyong et al, 2010). Obtain an ECG and institute continuous cardiac monitoring after large or deliberate ingestions.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: 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, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) LACK OF EFFECT
    1) No data suggest use of enhanced elimination.

Range Of Toxicity

Summary

    A) TOXICITY: A toxic dose has not been well established. Severity of intoxication should be based on clinical findings. These agents appear to have low systemic toxicity. The World Health Organization (WHO) has classified clopyralid, diflufenican, dithiopyr, florasulam, and fluroxypyr as Class U (unlikely to present acute hazard in normal use). Triclopyr is classified as Class III (slightly hazardous). Healthy volunteers have received 0.5 mg/kg of triclopyr safely. A 57-year-old man survived intentional ingestion of 300 mL of triclopyr (estimated ingested amount of triclopyr: 1500 mg/kg; 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, 65.5% water). Three patients survived after ingesting triclopyr 70% (doses: 5 mL, 40 mL, and 300 mL).

Maximum Tolerated Exposure

    A) WORLD HEALTH ORGANIZATION PESTICIDE CLASSIFICATION
    1) Pyridine herbicide WHO (World Health Organization) classifications (World Health Organization, 2006):
    1) Clopyralid (Dichloropicolinic acid): Class U (unlikely to present acute hazard in normal use)
    2) Diflufenican: Class U (unlikely to present acute hazard in normal use)
    3) Dithiopyr: Class U (unlikely to present acute hazard in normal use)
    4) Florasulam (pyroxsulam): Class U (unlikely to present acute hazard in normal use)
    5) Fluroxypyr: Class U (unlikely to present acute hazard in normal use)
    6) Haloxydine: Obsolete
    7) Triclopyr: Class III (slightly hazardous)
    B) TRICLOPYR
    1) In one study, medical records of 17 adult patients with acute herbicide auxin analogue (dicamba, triclopyr, MCPA or mecoprop) intoxication were identified. Three patients ingested triclopyr 70% in a solvent of 2-(2-(4-nonylphenoxy)ethoxy) ethanol 4.5%. One patient presented to the hospital 4 hours after ingesting 300 mL of triclopyr, another presented 7 hours after ingesting 40 mL, and a third patient presented 27 hours after ingesting 5 mL. All 3 patients survived exposure and were hospitalized for 5 days. Treatment was supportive in all cases and included hemodialysis and hemoperfusion (Park et al, 2011).
    2) ORAL: Six healthy volunteers experienced no adverse clinical effects during a triclopyr study or at 3 post-study examinations following single administrations of oral triclopyr at 0.1 mg/kg and 0.5 mg/kg of body weight. The dose was administered in apple juice at 0.176 mg/mL. Analytical grade triclopyr (3,5,6-trichloro-2-pyridinyloxyacetic acid) of 99.8% purity was used during the study (Carmichael et al, 1989).
    3) DERMAL: Five healthy volunteers experienced no adverse clinical effects during a triclopyr study or at 3 post-study examinations following dermal application of 0.65 to 1.1 mL of undiluted herbicide equivalent to triclopyr 5 mg/kg of body weight (Carmichael et al, 1989).
    4) A 57-year-old man with a history of hypertension and colon cancer developed coma, metabolic acidosis, hypotension, and ECG abnormalities after intentionally ingesting approximately 300 mL (estimated ingested amount of triclopyr: 1500 mg/kg) of triclopyr herbicide composed of 30% triclopyr triethylamine (T-TEA) salt, 4.5% polyoxyethylene nonylphenol surfactant, and 65.5% water. He received supportive treatment and recovered fully within 57 hours of ingestion (Kyong et al, 2010).

Workplace Standards

    A) ACGIH TLV Values for CAS55335-06-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) ACGIH TLV Values for CAS97886-45-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    C) ACGIH TLV Values for CAS1970-40-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    D) ACGIH TLV Values for CAS117718-60-2 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    E) ACGIH TLV Values for CAS69377-81-7 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    F) ACGIH TLV Values for CAS1702-17-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    G) NIOSH REL and IDLH Values for CAS55335-06-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    H) NIOSH REL and IDLH Values for CAS97886-45-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    I) NIOSH REL and IDLH Values for CAS1970-40-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    J) NIOSH REL and IDLH Values for CAS117718-60-2 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    K) NIOSH REL and IDLH Values for CAS69377-81-7 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    L) NIOSH REL and IDLH Values for CAS1702-17-6 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    M) Carcinogenicity Ratings for CAS55335-06-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    N) Carcinogenicity Ratings for CAS97886-45-8 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    O) Carcinogenicity Ratings for CAS1970-40-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    P) Carcinogenicity Ratings for CAS117718-60-2 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    Q) Carcinogenicity Ratings for CAS69377-81-7 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    R) Carcinogenicity Ratings for CAS1702-17-6 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) 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): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    S) OSHA PEL Values for CAS55335-06-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    T) OSHA PEL Values for CAS97886-45-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    U) OSHA PEL Values for CAS1970-40-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    V) OSHA PEL Values for CAS117718-60-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    W) OSHA PEL Values for CAS69377-81-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    X) OSHA PEL Values for CAS1702-17-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) CLOPYRALID
    1) LD50- (ORAL)MOUSE:
    a) >5 gm/kg(RTECS, 2003)
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 900 mg/kg
    3) LD50- (ORAL)RAT:
    a) 4300 mg/kg
    B) DITHIOPYR
    1) LD50- (ORAL)MOUSE:
    a) >5 gm/kg
    2) LD50- (ORAL)RAT:
    a) >5 mg/kg (RTECS, 2003)
    3) LD50- (SKIN)RAT:
    a) >5 mg/kg(RTECS, 2003)
    C) FLUROXYPYR
    1) LD50- (INTRAPERITONEAL)RAT:
    a) 458 mg/kg(RTECS, 2003)
    2) LD50- (ORAL)RAT:
    a) 2405 mg/kg(RTECS, 2003)
    3) LD50- (SKIN)RAT:
    a) >2 gm/kg(RTECS, 2003)
    D) PYRICLOR
    1) LD50- (ORAL)RAT:
    a) 80 mg/kg(RTECS, 2003)
    2) LD50- (SKIN)RAT:
    a) >2 gm/kg(RTECS, 2003)
    E) THIAZOPYR
    1) LD50- (ORAL)RAT:
    a) >5000 mg/kg(HSDB, 2003)
    2) LD50- (SKIN)RAT:
    a) >5000 mg/kg(HSDB, 2003)
    F) TRICLOPYR
    1) LD50- (ORAL)RAT:
    a) 630 mg/kg(RTECS, 2003)
    2) LD50- (ORAL)RAT:
    a) 713 mg/kg(Budavari, 1996a)

Pharmacology Toxicology

Pharmacologic Mechanism

    A) The mechanism of action for pyridine herbicides is by mimicking auxin, a natural growth inhibiting hormone in plants (Grossmann, 2007).

Toxicologic Mechanism

    A) Some dermal absorption does occur with regular use, resulting in detectable urine concentrations. This does not correlate with clinical symptoms (Cowell et al, 1991).

Physicochemical

Physical Characteristics

    A) Clopyralid is an odorless, white, crystalline solid(Budavari, 1996).
    B) Dithiopyr is a colorless crystalline solid with a faint odor(Budavari, 1996).
    C) Fluroxypyr is an odorless white crystalline solid(HSDB, 2003).
    D) Thiazopyr is a light tan granular or crystalline solid with a sulfurous odor(HSDB, 2003).
    E) Triclopyr is a fluffy solid substance(Lewis, 2000).

Molecular Weight

    1) Clopyralid: 192.00(RTECS, 2003)
    2) Dithiopyr: 401.44(RTECS, 2003)
    3) Fluroxypyr: 255.04(RTECS, 2003)
    4) Pyriclor: 198.43(RTECS, 2003)
    5) Thiazopyr 396.41(RTECS, 2003)
    6) Tricloppyr 256.47(RTECS, 2003)

References

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