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BENZOYLPHENYLUREA PESTICIDES

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Benzoylphenylurea pesticides are insect growth regulators. Their mode of action differs from contact pesticides that disrupt the insects nervous function. These agents are ingested by the insect and block chitin synthesis, compromising exoskeleton integrity. Chitin is the compound that causes the insect's outer covering to become hard, thus interfering with the formation of the insect's shell. The shell is not able to support the insect or withstand the rigors of molting. Benzoylurea pesticides are particularly effective when they are applied just prior to insect molting.

Specific Substances

    A) BISTRIFLURON
    1) N-[[[2-chloro-3,5-bis(trifluoromethyl)phenyl]amino]carbonyl] -2,6-difluorobenzamide
    2) 1-[2-chloro-3,5-bis(trifluoromethyl)phenyl]-3-(2,6-difluorobenzoyl)urea
    3) DBI-3204
    CHLORFLUAZURON
    1) Atabron
    2) Benzamide, N-((3,5-dichloro-4-((3-chloro-5-(trifluoromethyl)-2- pyridinyl)osy)phenyl)amino)carbonyl)-2,6-difluoro-
    3) CGA 112913
    4) IKI 7899
    5) PP 145
    6) UC 62644
    DIAFENTHIURON
    1) 1-tert-Butyl-3-(2,6-di-isopropyl-4-phenoxyphenyl)thiourea
    2) 3-(2,6-Diisopropyl-4-phenoxyphenyl)-1-tert-butylthiourea
    3) CGA 106630
    4) N-(2,6-Bis(1-methylethyl)-4-phenoxyphenyl)-N' -(1,1-dimethylethyl)thiourea
    5) Pegasus
    6) Polo
    7) Thiourea, N-(2,6-bis(1-methylethyl)-4-phenoxyphenyl)-N'-(1,1-dimethylethyl)-
    DIFLUBENZURON
    1) 1-(4-Chlorophenyl)-3-(2,6-difluorobenzoyl)urea
    2) Benzamide, N-(((4-chlorophenyl)amino)carbonyl)-2,6-difluoro-
    3) Difluron
    4) Dimilin
    5) DU 112307
    6) ENT 29054
    7) Largon
    8) Micromite
    9) N-(((4-Chlorophenyl)amino)carbonyl)-2,6-difluorobenzamide
    10) OMS 1804
    11) PDD 6040-1
    12) PH 60-40
    13) Philips-duphar PH 60-40
    14) TH 6040
    15) Thompson-hayward TH6040
    16) Urea, 1-(p-chlorophenyl)-3-(2,6-difluorobenzoyl)-
    FLUCYCLOXURON
    1) A 1335
    2) Andalin
    3) Benzamide, N-(((4-(((((4- chlorophenyl)cyclopropylmethylene)amino) oxy)methyl)phenyl)amino)carbonyl)-2,6-difluoro-
    4) DU 319722
    5) OMS 3041
    6) PH 70-23
    7) UBI-A 1335
    FLUFENOXURON
    1) Benzamide, N-(((4-(2-chloro-4-(trifluoromethyl)phenoxy) -2-fluorophenyl)amino)carbonyl)-2,6-difluoro-
    2) Cascade
    3) N-((4-(2-Chloro-4-(trifluoromethyl)phenoxy) -2-fluorophenyl)carbamoyl)-2,6-difluorobenzamide
    4) WL 115110
    HEXAFLUMURON
    1) 1-(3,5-Dichloro-4-(1,1,2,2-tetrafluoroethoxy)phenyl) -3-(2,6-difluorobenzoyl)urea (IUPAC)
    2) AI3-29832
    3) Benzamide, N-(((3,5-dichloro-4- (1,1,2,2-tetrafluoroethoxy)phenyl)amino)carbonyl) -2,6-difluoro-
    4) DE-473
    5) Hexafluron
    6) NAF-46
    7) Sonet
    8) XRD 473
    LUFENURON
    1) 1-[2,5-Dichloro-4-(1,1,2,3,3,3-hexafluoropropoxy)phenyl] -3-(2,6-difluorobenzoyl)urea
    2) Program
    3) CGA-184699
    NOVALURON
    1) 1-(3-chloro-4-(1,1,2-trifluoro-2-trifluoromethoxy-ethoxy)phenyl) -3-(2,6-difluorobenzoyl)urea
    2) Rimon
    NOVIFLUMURON
    1) N-[[[3,5-dichloro-2-fluoro-4-(1,1,2,3,3,3-hexafluoropropoxy) phenyl]amino]carbonyl]-2,6-difluorobenzamide
    2) Recruit III
    PENFLURON
    1) Benzamide, 2,6-difluoro-N-(((4-(trifluoromethyl)phenyl)amino)carbonyl)-
    2) Difluorobenzoyl-N'-(4-(trifluoromethyl)phenyl)urea
    3) Difluoro-N-(((4-(trifluoroethyl)phenyl)amino)carbonyl)benzamide
    4) PH 60-44
    5) Super diflubenzuron
    TEFLUBENZURON
    1) 1-(3,5-Dichloro-2,4-difluorophenyl)-3-(2,6-difluorobenzoyl)urea
    2) Benzamide, N-(((3,5-dichloro-2,4-difluorophenyl)amino)carbonyl)-2,6-difluoro-
    3) CME 134
    4) Dart
    5) Diaract
    6) HOE 522
    7) MK 139
    8) N-(((3,5-Dichloro-2,4-diflurophenyl)amino)carbonyl) -2,6-difluorobenzamide
    9) Nomolt
    10) Tefluron
    TRIFLUMURON
    1) 2-Chloro-N-(((4-(trifluoromethoxy)phenyl)amino)carbonyl)benzamide
    2) Alsystin
    3) Alsystine
    4) BAY-SIR 8514
    5) BAY-Vi 7533
    6) Benzamide, 2-chloro-N-(((4-(trifluoromethoxy)phenyl)amino)carbonyl)-
    7) Mascot
    8) Sir 8514
    9) Trifluron

    1.2.1) MOLECULAR FORMULA
    1) Bistrifluron: C16-H7-Cl-F8-N2-O2
    2) Chlorfluazuron: C20-H9-Cl3-F5-N3-O3
    3) Diafenthiuron: C23-H32-N2-O-S
    4) Diflubenzuron: C14-H9-Cl-F2-N2-O2
    5) Flucycloxuron: C25-H20-Cl-F2-N3-O3
    6) Hexaflumuron: C16-H8-Cl2-F6-N2-O3
    7) Lufenuron: C17-H8-Cl2-F8-N2-O4
    8) Novaluron: C17-H9-Cl-F8-N2-O4
    9) Noviflumuron: C17-H7-Cl2-F9-N2-O3
    10) Penfluron: C15-H9-F5-N2-O2
    11) Teflubenzuron: C14-H6-Cl2-F4-N2-O2
    12) Triflumuron: C15-H10-Cl-F3-N2-O3

Available Forms Sources

    A) FORMS
    1) The first benzoylureas were introduced in 1978 by Bayer of Germany (Ware, 1999).
    2) White or colorless crystalline solid. The technical material is off-white to yellow crystals(HSDB, 2003).
    3) DIFLUBENZURON - available as a suspension concentrate, wettable powder, or in granules or pellets (EXTOXNET, 1996). It is applied by airblast, aircraft or hydraulic sprayer.
    B) SOURCES
    1) Diflubenzuron is produced by the reaction of 2,6-difluorobenzamide with 4-chlorophenylisocyanate (IPCS, 1995).
    C) USES
    1) The benzoylphenyl ureas are insecticides and larvacides which act as insect growth regulators. They inhibit molting of larvae of mosquitoes, houseflies, stable flies and black flies by interfering with chitin synthesis.
    2) Diflubenzuron is used to control leaf eating insects such as gypsy moths, mosquito larvae, and rust mites that feed on agricultural, forest and ornamental plants. It is used primarily on cattle, citrus, cotton, mushrooms, ornamentals, standing water, forestry trees and in programs to control mosquito larvae and gypsy moth populations(EPA, 1997).
    3) Novaluron is recommended for the control of whiteflies, thrips, leafminers and army worms on containerized ornamentals grown in greenhouses (EPA, 2001).
    4) Hexaflumuron is a termiticide that was first registered in the United States in 1994. It is used for termite inspection, monitoring and baiting systems(NPTN, 2000).

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: Benzoylphenylurea pesticides are insect growth regulators.
    B) TOXICOLOGY: Their mode of action differs from contact pesticides that disrupt the insects nervous function. These agents are ingested by the insect and block chitin synthesis, compromising exoskeleton integrity. Chitin is the compound that causes the insect's outer covering to become hard, thus interfering with the formation of the insect's shell. The shell is not able to support the insect or withstand the rigors of molting. Benzoylurea pesticides are particularly effective when they are applied just prior to insect molting.
    C) EPIDEMIOLOGY: Exposure is rare.
    D) WITH POISONING/EXPOSURE
    1) CLINICAL TOXICITY: In healthy humans, the benzoylphenylurea insecticides are not considered to pose any significant toxicological risk, although human data are very limited. Most cases of human exposure are via dermal or inhalation contact resulting from aerial or hydraulic spraying or handling of the substance. Oral exposure may occur after ingesting residues of the chemicals in the diet. Vomiting has been reported in animals. Intentional ingestion of flufenoxuron-containing insecticides resulted in the development of lactic acidosis, shock, myocardial dysfunction, abdominal compartment syndrome leading to multiorgan failure and death in one adult. The diflubenzuron metabolite, 4-chloroaniline, has been reported to cause methemoglobinemia in workers exposed to the chemical and in neonates inadvertently exposed.
    0.2.20) REPRODUCTIVE
    A) Animal studies have not shown any adverse effects on fertility or reproduction.
    0.2.21) CARCINOGENICITY
    A) The US EPA has determined that there is no evidence of carcinogenicity for diflubenzuron, although p-chloroaniline, a metabolite of diflubenzuron is a probable human carcinogen .

Laboratory Monitoring

    A) Toxic serum concentrations of benzoylphenylurea insecticides are not clinically useful or readily available.
    B) Monitor vital signs and mental status following a significant exposure.
    C) Monitor CBC with differential in symptomatic patients. Obtain methemoglobin concentrations in all cyanotic patients and patients demonstrating dyspnea or other signs of hypoxia.
    D) Monitor fluid status and serum electrolytes in patients with symptoms of severe vomiting.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Limited exposure information. Symptomatic and supportive care are the mainstay of treatment for a benzoylphenylurea insecticide exposure. Manage mild hypotension with IV fluids.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. The diflubenzuron metabolite, 4-chloroaniline, has been reported to cause methemoglobinemia in workers exposed to the chemical and in neonates inadvertently exposed. Obtain a methemoglobin concentration in cyanotic patients. Treat symptomatic methemoglobinemia (usually at methemoglobin concentrations above 20% to 30%) with methylene blue and oxygen therapy.
    C) NATIONAL PESTICIDE TELECOMMUNICATIONS NETWORK
    1) The National Pesticide Information Center (NPIC) is a cooperative effort of Oregon State University and the US EPA. NPIC provides consultation to poison centers and other health care professionals for the management of pesticide poisoning. Calls regarding emergency cases requiring immediate medical response will be transferred to the Oregon Poison Center.
    a) NPIC contact information: phone: 1-800-858-7378. email: npic@ace.orst.edu Hours: 8 AM to 12 PM Pacific time Monday through Friday, excluding holidays.
    D) DECONTAMINATION
    1) PREHOSPITAL: Observe patients with large ingestions for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary. Remove clothing and wash exposed areas with soap and water. If ocular exposure develops, irrigate thoroughly. Consider activated charcoal only after a large, recent ingestion in patients who are alert and can protect their airway. Following an inhalational exposure, move patient to fresh air.
    2) HOSPITAL: Consider activated charcoal only after a large, recent ingestion in patients who are alert and can protect their airway. If prehospital decontamination has not occurred, wash exposed skin and irrigate exposed eyes thoroughly as necessary.
    E) AIRWAY MANAGEMENT
    1) Ensure adequate ventilation and perform endotracheal intubation early in patients with severe respiratory distress or methemoglobinemia and severe dyspnea.
    F) ANTIDOTE
    1) There is no known antidote. Treat methemoglobinemia with methylene blue.
    G) METHEMOGLOBINEMIA
    1) Initiate oxygen therapy. Treat with methylene blue if patient is symptomatic (usually at methemoglobin concentrations greater than 20% to 30% or at lower concentrations in patients with anemia, underlying pulmonary or cardiovascular disease). METHYLENE BLUE: INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules and 10 mg/1 mL (1% solution) vials. Additional doses may sometimes be required. Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection. NEONATES: DOSE: 0.3 to 1 mg/kg.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with a deliberate exposure, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.
    3) ADMISSION CRITERIA: Patients with severe symptoms despite treatment should be admitted.
    4) CONSULT CRITERIA: Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    I) PITFALLS
    1) Missing an ingestion of another chemical or other possible etiologies for a patient’s symptoms. History of exposure may be difficult to obtain in some settings.
    J) TOXICOKINETICS
    1) These agents can be absorbed by humans in work situations dermally or by inhalation. Diflubenzuron is widely distributed in the tissues, but it does not accumulate.
    K) DIFFERENTIAL DIAGNOSIS
    1) Other herbicides, fungicides, or insecticides. Other methemoglobin inducing agents such as aniline dyes, dapsone, or benzocaine.
    0.4.3) INHALATION EXPOSURE
    A) 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.
    0.4.4) EYE EXPOSURE
    A) 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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: Toxic levels for humans have not been established. One case of intentional ingestion of 100 mL of a pesticide containing 5.3% flufenoxuron resulted in development of lactic acidosis, shock, abdominal compartment syndrome leading to multiorgan failure and subsequent death. In another case, ingestion of 8321 mg flufenoxuron (110.95 mg/kg) in a 54-year-old man resulted in lactic acidosis, shock, and transient myocardial dysfunction (elevated cardiac enzymes, global left ventricular hypokinesia) with eventual recovery following supportive care.

Clinical Effects

Summary Of Exposure

    A) USES: Benzoylphenylurea pesticides are insect growth regulators.
    B) TOXICOLOGY: Their mode of action differs from contact pesticides that disrupt the insects nervous function. These agents are ingested by the insect and block chitin synthesis, compromising exoskeleton integrity. Chitin is the compound that causes the insect's outer covering to become hard, thus interfering with the formation of the insect's shell. The shell is not able to support the insect or withstand the rigors of molting. Benzoylurea pesticides are particularly effective when they are applied just prior to insect molting.
    C) EPIDEMIOLOGY: Exposure is rare.
    D) WITH POISONING/EXPOSURE
    1) CLINICAL TOXICITY: In healthy humans, the benzoylphenylurea insecticides are not considered to pose any significant toxicological risk, although human data are very limited. Most cases of human exposure are via dermal or inhalation contact resulting from aerial or hydraulic spraying or handling of the substance. Oral exposure may occur after ingesting residues of the chemicals in the diet. Vomiting has been reported in animals. Intentional ingestion of flufenoxuron-containing insecticides resulted in the development of lactic acidosis, shock, myocardial dysfunction, abdominal compartment syndrome leading to multiorgan failure and death in one adult. The diflubenzuron metabolite, 4-chloroaniline, has been reported to cause methemoglobinemia in workers exposed to the chemical and in neonates inadvertently exposed.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) SHOCK
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 66-year-old man developed lactic acidosis and circulatory shock (blood pressure 84/47 mmHg), after intentionally ingesting 100 mL of a pesticide containing flufenoxuron 5.3%, polyoxyethylene nonylphenol 8%, N-methyl-2-pyrrolidone 20%, ethoxylated nonylphenol phosphate 10%, and cyclohexanone 56.7%. With supportive therapy, including vasopressor administration and initiation of continuous venovenous hemodiafiltration, the patient's metabolic acidosis and hemodynamic status improved; however, on hospital day 7, the patient experienced a tense and distended abdomen, with a decrease in urine output (less than 10 mL/hour) and an increase in serum creatinine concentration (2.7 mg/dL). An abdominal CT scan revealed ascites in the abdomen with diffuse bowel wall swelling, and intra-abdominal pressure monitoring was elevated (greater than 20 mmHg), indicating abdominal compartment syndrome. Over the next several days, the patient's condition continued to deteriorate and he died of multiple organ failure on hospital day 19 (Choi et al, 2011).
    b) CASE REPORT: Lactic acidosis, shock (blood pressure 40/20 mmHg), and transient myocardial dysfunction (elevated cardiac enzymes, global left ventricular hypokinesia) occurred in a 54-year-old man following ingestion of an insecticide containing 5.3% flufenoxuron. Total amount of flufenoxuron ingested was approximately 8321 mg (110.95 mg/kg). The patient gradually recovered following supportive therapy, including sodium bicarbonate and vasopressor (norepinephrine, dopamine) administration (Woo & Lim, 2015).
    B) MYOCARDIAL DYSFUNCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 54-year-old man developed lactic acidosis, shock (initial blood pressure 40/20 mmHg), and myocardial dysfunction following ingestion of an insecticide containing 5.3% flufenoxuron. Total amount of flufenoxuron ingested was approximately 8321 mg (110.95 mg/kg). Initially, at presentation (approximately 1 hour postingestion), the patient's creatine phosphokinase, troponin I, and CK-MB levels were normal. However, 9 hours later, his creatine phosphokinase level peaked at 4488 Units/liter (15.26 times the upper reference limit [URL]). Twenty-four hours after initial levels were drawn, his troponin I level and his CK-MB level peaked at 2.086 ng/mL (2.67 times the URL) and 37.45 ng/mL (7.49 times the URL), respectively. After 70 hours, the patient's cardiac enzyme levels normalized. In addition, an echocardiography revealed global left ventricular hypokinesia and a left ventricular ejection fraction of 40%. A repeat echocardiography, performed 45 hours later, was normal. With supportive therapy, including sodium bicarbonate and vasopressor (norepinephrine, dopamine) administration, the patient recovered and was discharged on hospital day 6 refusing any further testing such as a coronary angiography (Woo & Lim, 2015).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY CONDITION DUE TO CHEMICAL FUMES AND/OR VAPORS
    1) WITH POISONING/EXPOSURE
    a) Sneezing, nasal irritation and congestion, chest tightness, difficulty breathing, cough, and impaired lung function have been reported, but these are probably related to the addition of wood flour (cellulose) in this product (MSDS, 1996).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) ABDOMINAL COMPARTMENT SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 66-year-old man developed lactic acidosis and circulatory shock after intentionally ingesting 100 mL of a pesticide containing flufenoxuron 5.3%, polyoxyethylene nonylphenol 8%, N-methyl-2-pyrrolidone 20%, ethoxylated nonylphenol phosphate 10%, and cyclohexanone 56.7%. With supportive therapy, including vasopressor administration and initiation of continuous venovenous hemodiafiltration, the patient's metabolic acidosis and hemodynamic status improved; however, on hospital day 7, the patient experienced a tense and distended abdomen, with a decrease in urine output (less than 10 mL/hour) and an increase in serum creatinine concentration (2.7 mg/dL). An abdominal CT scan revealed ascites in the abdomen with diffuse bowel wall swelling, and intra-abdominal pressure monitoring was elevated (greater than 20 mmHg), indicating abdominal compartment syndrome. Over the next several days, the patient's condition continued to deteriorate and he died of multiple organ failure on hospital day 19 (Choi et al, 2011).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) Nausea and vomiting
    a) Nausea and vomiting were seen after dogs were fed diafenthiuron 360 mg/kg for 90 days continually (RTECS, 2003).
    2) Splenomegaly
    a) In chronic rat feeding studies, rats that were given moderate amounts of diflubenzuron for 2 years had enlarged spleens. Mice in a similar study had liver and spleen enlargement at slightly lower levels of exposure (EXTOXNET, 1996).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) LACTIC ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 66-year-old man developed lactic acidosis (pH 7.11, PaO2 284.9 mmHg, PaCO2 35.8 mmHg, base excess -19.8 mmol/L, HCO3 11 mmol/L, lactic acid level 9.12 mmol/L) and circulatory shock after intentionally ingesting 100 mL of a pesticide containing flufenoxuron 5.3%, polyoxyethylene nonylphenol 8%, N-methyl-2-pyrrolidone 20%, ethoxylated nonylphenol phosphate 10%, and cyclohexanone 56.7%. With supportive therapy, including vasopressor administration and initiation of continuous venovenous hemodiafiltration, the patient's lactic acidosis and hemodynamic status improved; however, on hospital day 7, the patient experienced a tense and distended abdomen, with a decrease in urine output (less than 10 mL/hour) and an increase in serum creatinine concentration (2.7 mg/dL). An abdominal CT scan revealed ascites in the abdomen with diffuse bowel wall swelling, and intra-abdominal pressure monitoring was elevated (greater than 20 mmHg), indicating abdominal compartment syndrome. Over the next several days, the patient's condition continued to deteriorate and he died of multiple organ failure on hospital day 19 (Choi et al, 2011).
    b) CASE REPORT: A 54-year-old man developed lactic acidosis (pH 7.01, HCO3 7.7 mmol/L, lactate level 15 mmol/L) following ingestion of an insecticide containing 5.3% flufenoxuron. Total amount of flufenoxuron ingested was approximately 8321 mg (110.95 mg/kg). Following sodium bicarbonate therapy, the patient's acid base balance normalized approximately 15 hours postingestion (Woo & Lim, 2015).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) METHEMOGLOBINEMIA
    1) WITH POISONING/EXPOSURE
    a) The diflubenzuron metabolite, 4-chloroaniline, has been reported to cause methemoglobinemia in workers exposed to the chemical and in neonates inadvertently exposed. Some individuals deficient in NADH-methemoglobin reductase may be particularly sensitive to 4-chloroaniline and exposure to diflubenzuron (IPCS, 1995).
    b) The sensitivity of human hemoglobin to methemoglobin formation by 4-chloroaniline in vivo is not known.
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) METHEMOGLOBINEMIA
    a) Methemoglobinemia and sulfhemoglobinemia were observed in dogs fed diflubenzuron in a 1-year chronic feeding study. The dogs were administered 0, 2, 10, 50, and 250 mg/kg/day with the no-observed-effect level (NOEL) noted to be at 2 mg/kg/day. Methemoglobinemia was observed at 10 mg/kg/day. Hemolytic anemia, erythrocyte destruction, and compensatory erythrocyte regeneration were observed at the 50 mg/kg/day or higher dosage levels (Anon, 1996).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Novaluron is not a dermal irritant and does not cause skin sensitization (EPA, 2001).

Reproductive

    3.20.1) SUMMARY
    A) Animal studies have not shown any adverse effects on fertility or reproduction.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) No teratogenic or fetotoxic effects were seen in rats at levels up to 4 mg/kg body weight per day (HSDB, 2003).
    3.20.5) FERTILITY
    A) ANIMAL STUDIES
    1) LACK OF EFFECT
    a) Female and male layer-breed chickens were tested from day one of age through a laying cycle at levels of 1, 2.5, 25, and 250 ppm diflubenzuron in the feed. Egg production, egg weight, eggshell weight, fertility, hatchability and effects on the progeny were not affected, even at the 250 ppm level (Kubena, 1982).
    b) In a three generational rat study, no adverse effects were seen on reproductive performance at 160 ppm (8 mg/kg/day), the highest dose tested (HSDB, 2003).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS35367-38-5 (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 CAS51026-04-1 (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 CAS86479-0603 (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 CAS116714-46-6 (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
    3.21.2) SUMMARY/HUMAN
    A) The US EPA has determined that there is no evidence of carcinogenicity for diflubenzuron, although p-chloroaniline, a metabolite of diflubenzuron is a probable human carcinogen .
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Diflubenzuron was not found to cause cancer in male and female mice at doses up to 10,000 ppm (500 mg/kg body weight per day)(HSDB, 2003).
    2) In a 104 week carcinogenicity study of technical grade diflubenzuron administered to rats in doses up to 500 mg/kg/day, increases in methemoglobin and suflhemoglobin were seen at all levels. No incidence of increased incidence of neoplastic lesions were seen in either male or female rats(EPA, 1997).

Genotoxicity

    A) Benzoylphenyl urea pesticides have not been found to be mutagenic or cause adverse genetic effects in animal studies.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Toxic serum concentrations of benzoylphenylurea insecticides are not clinically useful or readily available.
    B) Monitor vital signs and mental status following a significant exposure.
    C) Monitor CBC with differential in symptomatic patients. Obtain methemoglobin concentrations in all cyanotic patients and patients demonstrating dyspnea or other signs of hypoxia.
    D) Monitor fluid status and serum electrolytes in patients with symptoms of severe vomiting.

Methods

    A) Liquid chromatography or gas liquid chromatography are the methods of choice for determining the presence of diflubenzuron in pesticide formulations (HSDB, 2003).
    B) Gas or liquid chromatography with electron capture detection, high performance liquid chromatography with spectrometric detection, and enzyme-linked immunosorbent assay methods are all available diflubenzuron residue assay methods (U.S. Dept of Agriculture, 1995).

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 severe symptoms despite treatment should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent exposure, that remains asymptomatic can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a regional poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a deliberate exposure, and those who are symptomatic, need to be monitored until they are clearly improving and clinically stable.

Monitoring

    A) Toxic serum concentrations of benzoylphenylurea insecticides are not clinically useful or readily available.
    B) Monitor vital signs and mental status following a significant exposure.
    C) Monitor CBC with differential in symptomatic patients. Obtain methemoglobin concentrations in all cyanotic patients and patients demonstrating dyspnea or other signs of hypoxia.
    D) Monitor fluid status and serum electrolytes in patients with symptoms of severe vomiting.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Observe patients with large ingestions for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary. Remove clothing and wash exposed areas with soap and water. If ocular exposure develops, irrigate thoroughly. Consider activated charcoal only after large, recent ingestions in patients who are alert and can protect the airway. Following an inhalational exposure, move patient to fresh air.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) 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).
    1) 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.
    2) 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).
    2) 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).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Consider activated charcoal only after large, recent ingestions in patients who are alert and can protect their airway. If prehospital decontamination has not occurred, wash exposed skin and irrigate exposed eyes thoroughly.
    B) ACTIVATED CHARCOAL
    1) 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.
    2) 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) Limited exposure information. Symptomatic and supportive care are the mainstay of treatment for a benzoylphenylurea insecticide exposure. Manage mild hypotension with IV fluids.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Treat severe hypotension with IV 0.9% NaCl at 10 to 20 mL/kg. Add dopamine or norepinephrine if unresponsive to fluids. The diflubenzuron metabolite, 4-chloroaniline, has been reported to cause methemoglobinemia in workers exposed to the chemical and in neonates inadvertently exposed. Obtain a methemoglobin concentration in cyanotic patients. Treat symptomatic methemoglobinemia (usually at methemoglobin concentrations above 20% to 30%) with methylene blue and oxygen therapy.
    B) MONITORING OF PATIENT
    1) Toxic serum concentrations of benzoylphenylurea insecticides are not clinically useful or readily available.
    2) Monitor vital signs and mental status following a significant exposure.
    3) Monitor CBC with differential in symptomatic patients. Obtain methemoglobin concentrations in all cyanotic patients and patients demonstrating dyspnea or other signs of hypoxia.
    4) Monitor fluid status and serum electrolytes in patients with symptoms of severe vomiting.
    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) METHEMOGLOBINEMIA
    1) The diflubenzuron metabolite, 4-chloroaniline, has been reported to cause methemoglobinemia in workers exposed to the chemical and in neonates inadvertently exposed. Some individuals deficient in NADH-methemoglobin reductase may be particularly sensitive to 4-chloroaniline and exposure to diflubenzuron (IPCS, 1995).
    2) SUMMARY
    a) Determine the methemoglobin concentration and evaluate the patient for clinical effects of methemoglobinemia (ie, dyspnea, headache, fatigue, CNS depression, tachycardia, metabolic acidosis). Treat patients with symptomatic methemoglobinemia with methylene blue (this usually occurs at methemoglobin concentrations above 20% to 30%, but may occur at lower methemoglobin concentrations in patients with anemia, or underlying pulmonary or cardiovascular disorders). Administer oxygen while preparing for methylene blue therapy.
    3) METHYLENE BLUE
    a) INITIAL DOSE/ADULT OR CHILD: 1 mg/kg IV over 5 to 30 minutes; a repeat dose of up to 1 mg/kg may be given 1 hour after the first dose if methemoglobin levels remain greater than 30% or if signs and symptoms persist. NOTE: Methylene blue is available as follows: 50 mg/10 mL (5 mg/mL or 0.5% solution) single-dose ampules (Prod Info PROVAYBLUE(TM) intravenous injection, 2016) and 10 mg/1 mL (1% solution) vials (Prod Info methylene blue 1% intravenous injection, 2011). REPEAT DOSES: Additional doses may be required, especially for substances with prolonged absorption, slow elimination, or those that form metabolites that produce methemoglobin. NOTE: Large doses of methylene blue may cause methemoglobinemia or hemolysis (Howland, 2006). Improvement is usually noted shortly after administration if diagnosis is correct. Consider other diagnoses or treatment options if no improvement has been observed after several doses. If intravenous access cannot be established, methylene blue may also be given by intraosseous infusion. Methylene blue should not be given by subcutaneous or intrathecal injection (Prod Info methylene blue 1% intravenous injection, 2011; Herman et al, 1999). NEONATES: DOSE: 0.3 to 1 mg/kg (Hjelt et al, 1995).
    b) CONTRAINDICATIONS: G-6-PD deficiency (methylene blue may cause hemolysis), known hypersensitivity to methylene blue, methemoglobin reductase deficiency (Shepherd & Keyes, 2004)
    c) FAILURE: Failure of methylene blue therapy suggests: inadequate dose of methylene blue, inadequate decontamination, NADPH dependent methemoglobin reductase deficiency, hemoglobin M disease, sulfhemoglobinemia, or G-6-PD deficiency. Methylene blue is reduced by methemoglobin reductase and nicotinamide adenosine dinucleotide phosphate (NADPH) to leukomethylene blue. This in turn reduces methemoglobin. Red blood cells of patients with G-6-PD deficiency do not produce enough NADPH to convert methylene blue to leukomethylene blue (do Nascimento et al, 2008).
    d) DRUG INTERACTION: Concomitant use of methylene blue with serotonergic drugs, including serotonin reuptake inhibitors (SRIs), selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), norepinephrine-dopamine reuptake inhibitors (NDRIs), triptans, and ergot alkaloids may increase the risk of potentially fatal serotonin syndrome (U.S. Food and Drug Administration, 2011; Stanford et al, 2010; Prod Info methylene blue 1% IV injection, 2011).
    4) TOLUIDINE BLUE OR TOLONIUM CHLORIDE (GERMANY)
    a) DOSE: 2 to 4 mg/kg intravenously over 5 minutes. Dose may be repeated in 30 minutes (Nemec, 2011; Lindenmann et al, 2006; Kiese et al, 1972).
    b) SIDE EFFECTS: Hypotension with rapid intravenous administration. Vomiting, diarrhea, excessive sweating, hypotension, dysrhythmias, hemolysis, agranulocytosis and acute renal insufficiency after overdose (Dunipace et al, 1992; Hix & Wilson, 1987; Winek et al, 1969; Teunis et al, 1970; Marquez & Todd, 1959).
    c) CONTRAINDICATIONS: G-6-PD deficiency; may cause hemolysis.

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) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

Summary

    A) TOXICITY: Toxic levels for humans have not been established. One case of intentional ingestion of 100 mL of a pesticide containing 5.3% flufenoxuron resulted in development of lactic acidosis, shock, abdominal compartment syndrome leading to multiorgan failure and subsequent death. In another case, ingestion of 8321 mg flufenoxuron (110.95 mg/kg) in a 54-year-old man resulted in lactic acidosis, shock, and transient myocardial dysfunction (elevated cardiac enzymes, global left ventricular hypokinesia) with eventual recovery following supportive care.

Minimum Lethal Exposure

    A) CASE REPORT: A 66-year-old man developed lactic acidosis and circulatory shock after intentionally ingesting 100 mL of a pesticide containing flufenoxuron 5.3%, polyoxyethylene nonylphenol 8%, N-methyl-2-pyrrolidone 20%, ethoxylated nonylphenol phosphate 10%, and cyclohexanone 56.7%. With supportive therapy, including vasopressor administration and initiation of continuous venovenous hemodiafiltration, the patient's metabolic acidosis and hemodynamic status improved; however, on hospital day 7, the patient experienced a tense and distended abdomen, with a decrease in urine output (less than 10 mL/hour) and an increase in serum creatinine concentration (2.7 mg/dL). An abdominal CT scan revealed ascites in the abdomen with diffuse bowel wall swelling and intra-abdominal pressure monitoring was elevated (greater than 20 mmHg) indicating abdominal compartment syndrome. Over the next several days, the patient's condition continued to deteriorate and he died of multiple organ failure on hospital day 19 (Choi et al, 2011).

Maximum Tolerated Exposure

    A) CASE REPORT: Lactic acidosis, shock (blood pressure 40/20 mmHg), and transient myocardial dysfunction (elevated cardiac enzymes, global left ventricular hypokinesia) occurred in a 54-year-old man following ingestion of an insecticide containing 5.3% flufenoxuron. The total amount of flufenoxuron ingested was approximately 8321 mg (110.95 mg/kg). The patient gradually recovered following supportive therapy, including sodium bicarbonate and vasopressor (norepinephrine, dopamine) administration (Woo & Lim, 2015).

Workplace Standards

    A) ACGIH TLV Values for CAS35367-38-5 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) ACGIH TLV Values for CAS51026-04-1 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    C) ACGIH TLV Values for CAS86479-0603 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    D) ACGIH TLV Values for CAS116714-46-6 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    E) NIOSH REL and IDLH Values for CAS35367-38-5 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    F) NIOSH REL and IDLH Values for CAS51026-04-1 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    G) NIOSH REL and IDLH Values for CAS86479-0603 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    H) NIOSH REL and IDLH Values for CAS116714-46-6 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    I) Carcinogenicity Ratings for CAS35367-38-5 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Diflubenzuron
    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

    J) Carcinogenicity Ratings for CAS51026-04-1 :
    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

    K) Carcinogenicity Ratings for CAS86479-0603 :
    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

    L) Carcinogenicity Ratings for CAS116714-46-6 :
    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

    M) OSHA PEL Values for CAS35367-38-5 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    N) OSHA PEL Values for CAS51026-04-1 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    O) OSHA PEL Values for CAS86479-0603 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    P) OSHA PEL Values for CAS116714-46-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) CHLORFLUAZURON
    1) LD50- (ORAL)MOUSE:
    a) 350 mg/kg (RTECS, 2003)
    2) LD50- (ORAL)RAT:
    a) 445 mg/kg(RTECS, 2003)
    3) LD50- (SKIN)RAT:
    a) 720 mg/kg (RTECS, 2003)
    B) DIAFENTHIURON
    1) LD50- (ORAL)RAT:
    a) 2068 mg/kg (RTECS, 2003)
    2) LD50- (SKIN)RAT:
    a) greater than 2 gm/kg (RTECS, 2003)
    C) DIFLUBENZURON
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 2150 mg/kg (RTECS, 2003)
    2) LD50- (ORAL)MOUSE:
    a) 4640 mg/kg (RTECS, 2003)
    3) LD50- (SKIN)MOUSE:
    a) greater than 6200 mg/kg (RTECS, 2003)
    4) LD50- (SUBCUTANEOUS)MOUSE:
    a) greater than 4 gm/kg (RTECS, 2003)
    5) LD50- (INTRAPERITONEAL)RAT:
    a) greater than 7500 mg/kg (RTECS, 2003)
    6) LD50- (ORAL)RAT:
    a) greater than 4640 mg/kg (RTECS, 2003)
    7) LD50- (SKIN)RAT:
    a) greater than 10 gm/kg (RTECS, 2003)
    8) LD50- (SUBCUTANEOUS)RAT:
    a) greater than 3400 mg/kg (RTECS, 2003)
    D) FLUCYCLOXURON
    1) LD50- (ORAL)RAT:
    a) greater than 5 gm/kg (RTECS, 2003)
    2) LD50- (SKIN)RAT:
    a) greater than 2 gm/kg (RTECS, 2003)
    E) FLUFENOXURON
    1) LD50- (ORAL)RAT:
    a) greater than 3 gm/kg (RTECS, 2003)
    2) LD50- (SKIN)RAT:
    a) greater than 2 gm/kg
    F) HEXAFLUMURON
    1) LD50- (ORAL)RAT:
    a) greater than 5 gm/kg (RTECS, 2003)
    2) LD50- (SKIN)RAT:
    a) greater than 5 gm/kg (RTECS, 2003)
    G) TEFLUBENZURON
    1) LD50- (ORAL)MOUSE:
    a) greater than 5 gm/kg (RTECS, 2003)
    2) LD50- (ORAL)RAT:
    a) greater than 5 gm/kg (RTECS, 2003)
    3) LD50- (SKIN)RAT:
    a) greater than 2 gm/kg (RTECS, 2003)
    H) TRIFLUMURON
    1) LD50- (ORAL)MOUSE:
    a) greater than 5 gm/kg (RTECS, 2003)
    2) LD50- (SUBCUTANEOUS)MOUSE:
    a) greater than 5 gm/kg (RTECS, 2003)
    3) LD50- (INTRAPERITONEAL)RAT:
    a) greater than 5 gm/kg (RTECS, 2003)
    4) LD50- (ORAL)RAT:
    a) greater than 5 gm/kg (RTECS, 2003)
    5) LD50- (SKIN)RAT:
    a) greater than 5 gm/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Benzoylphenyl urea pesticides disrupt the synthesis of chitin after they are ingested by insects.
    B) ANIMAL TOXICOLOGY
    1) Benzoylphenyl urea pesticides act as insect growth regulators or chitin synthesis inhibitors. They act on the larval stages of most insects and inhibit or block the synthesis of chitin. Chitin is the compound that causes the insect’s outer covering to become hard, thus interfering with the formation of the insect’s shell. The shell is not able to support the insect or withstand the rigors of molting. Typical effects on larvae are the rupture of malformed cuticle or death by starvation. An example is adult female boll weevils that are exposed to diflubenzuron lay eggs that do not hatch. Benzoylurea pesticides are particularly effective when they are applied just prior to insect molting.

Physicochemical

Physical Characteristics

    A) Diflubenzuron occurs as a white, crystalline solid or colorless crystals (EXTOXNET, 1996; HSDB, 2003).

Molecular Weight

    1) Chlorfluazuron: 540.6604
    2) Diafenthiuron: 384.5786
    3) Diflubenzuron: 310.6871
    4) Flucycloxuron: 483.9011
    5) Flufenoxuron: 488.7729
    6) Hexaflumuron: 461.1
    7) Lufenuron: 511.155
    8) Novaluron: 492.7093
    9) Penfluron: 344.2403
    10) Teflubenzuron: 381.1132
    11) Triflumuron: 358.7038

References

General Bibliography

    1) 40 CFR 372.28: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Lower thresholds for chemicals of special concern. National Archives and Records Administration (NARA) and the Government Printing Office (GPO). Washington, DC. Final rules current as of Apr 3, 2006.
    2) 40 CFR 372.65: Environmental Protection Agency - Toxic Chemical Release Reporting, Community Right-To-Know, Chemicals and Chemical Categories to which this part applies. National Archives and Records Association (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Apr 3, 2006.
    3) 49 CFR 172.101 - App. B: Department of Transportation - Table of Hazardous Materials, Appendix B: List of Marine Pollutants. National Archives and Records Administration (NARA) and the Government Printing Office (GPO), Washington, DC. Final rules current as of Aug 29, 2005.
    4) 62 FR 58840: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 1997.
    5) 65 FR 14186: Notice of the National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances - Proposed AEGL Values, Environmental Protection Agency, NAC/AEGL Committee. National Archives and Records Administration (NARA) and the Government Publishing Office (GPO), Washington, DC, 2000.
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