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ACETOXYTRIPHENYLSTANNANE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Acetoxytriphenylstannane is an alkyl tin compound.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C20-H18-O2-Sn

Available Forms Sources

    A) FORMS
    1) Acetoxytriphenylstannane, also called TRIPHENYLTIN ACETATE, is an alkyl tin compound. It occurs as colorless crystals or a white crystalline solid which is soluble in methylene chloride, is slightly soluble in ethanol or toluene, and is minimally soluble in water (HSDB , 2000).
    2) It is available as a wettable powder and a technical product of at least 94 percent purity (HSDB , 2000).
    B) USES
    1) Triphenyltin acetate is used as a fungicide, algicide, and wood preservative (HSDB , 2000; Lewis, 1996).
    2) Organotin compounds will attack some types of rubber, plastics, or coatings (HSDB , 2000); the selection of protective clothing should be done with care.

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Acetoxytriphenylstannane (triphenyltin acetate) is a trialkyl organotin compound. It is a colorless to white needle-like crystalline solid that is practically insoluble in water, and is used as a fungicide, algicide, and wood preservative. It can be absorbed systemically following ingestion, inhalation, and dermal contact, and is a skin irritant.
    1) Acetoxytriphenylstannane is available as a wettable powder and a technical product of at least 94 percent purity.
    2) Triphenyltin acetate has caused hepatic injury with irreversible hepatomegaly and elevated liver function tests with chronic occupational exposure. It also caused skin irritation with pruritus and erythema which developed 2 to 3 days after prolonged dermal contact with contaminated garments. Eye irritation has also occurred.
    a) Triphenyltin acetate may also cause blurred vision, headache, dizziness, loss of consciousness, malaise, visual disturbances, shortness of breath, epigastric pain, nausea, vomiting, and diarrhea. Glycosuria and hyperglycemia have been described.
    3) Because the group of ORGANOTIN compounds have a number of toxic effects IN COMMON, the following discussion deals with VARIOUS ORGANOTIN COMPOUNDS.
    0.2.4) HEENT
    A) Blurred vision, nystagmus, irritation, and photophobia have been described.
    B) Long-term sequelae of acute poisoning have included visual abnormalities.
    C) Tinnitus or deafness may occur, particularly following ingestion.
    D) Symptoms of trialkyl tin intoxication include nasal irritation.
    0.2.6) RESPIRATORY
    A) Respiratory tract irritation and cough have occurred with occupational organotin exposure. Systemic organotin poisoning has occurred following inhalation exposure. Respiratory depression may occur, particularly following ingestion. Symptoms of trialkyl tin intoxication include shortness of breath.
    0.2.7) NEUROLOGIC
    A) Encephalopathy, confusion, coma, sensorimotor polyneuropathy, headache, nausea, EEG changes, dizziness, vertigo, disorientation, psychosis, and weakness or flaccid paralysis of the limbs may occur, particularly following ingestion.
    B) Cerebral edema has been described following exposure to certain organotin compounds. Seizures and a diffuse sensation of pain may occur. Tremors may be noted.
    C) Long-term sequelae of acute poisoning have included paresthesias, headaches, visual abnormalities, aggressive behavior, memory deficits, and extrapyramidal hyperkinesis.
    0.2.8) GASTROINTESTINAL
    A) Abdominal pain, diarrhea, retching, nausea, and vomiting have been reported after triphenyltin ingestion.
    B) Based on their other irritant properties, organotin compounds would be predicted to cause esophageal or gastrointestinal tract irritation or burns following ingestion.
    0.2.9) HEPATIC
    A) Hepatic necrosis and hepatomegaly have been described following exposure to certain organotin compounds. Laboratory abnormalities in organotin poisoning include elevated liver function tests.
    0.2.10) GENITOURINARY
    A) Urinary retention or increased BUN may occur.
    B) Nephropathy has been reported.
    0.2.12) FLUID-ELECTROLYTE
    A) Laboratory abnormalities in organotin poisoning include hypokalemia.
    0.2.13) HEMATOLOGIC
    A) Laboratory abnormalities in organotin poisoning include leukocytosis and leukopenia.
    0.2.14) DERMATOLOGIC
    A) Organotin compounds are primary skin irritants and can be absorbed through intact skin. Skin lesions and itching occurred with occupational organotin exposure. Symptoms of trialkyl tin intoxication include possible skin burns, erythema, or dermatitis.
    0.2.15) MUSCULOSKELETAL
    A) Weakness or flaccid paralysis of the limbs may occur, particularly following ingestion.
    0.2.16) ENDOCRINE
    A) Metabolic abnormalities including increased blood sugar (due to centrally mediated depletion of catecholamines) may occur.
    0.2.18) PSYCHIATRIC
    A) Psychosis may occur, particularly following ingestion. Long-term sequelae of acute poisoning have included paresthesias, headaches, visual abnormalities, aggressive behavior, memory deficits, and extrapyramidal hyperkinesis.
    0.2.20) REPRODUCTIVE
    A) Teratogenicity from tin itself was not observed in animal studies. Triphenyltin itself was not teratogenic in rats.
    1) Specific developmental abnormalities in the musculoskeletal system, post-implantation mortality, change in litter size, behavior and weaning index have been noted in the offspring of rats administered Acetoxytriphenylstannane.
    a) In one rat study, acetoxytriphenylstannane was NOT teratogenic to the offspring, although a dose-dependent weight reduction in weight gain was observed in females. Behavioral changes have been noted in the pups of female rats fed acetoxytriphenylstannane during gestation.
    B) Acetoxytriphenylstannane caused a decrease in ovulation and female fertility in rats
    C) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    D) Toxic effects on the testes, epididymis and sperm duct have been observed in rat studies. Marked testicular atrophy developed in rats fed 20 mg/kg/day of acetoxytriphenylstannane for 20 days.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no studies were found on the possible carcinogenic activity of triphenyltin acetate in humans.

Laboratory Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) The average blood tin concentration in normal individuals is 0.14 mg/L; some normal individuals do not have detectable tin in the blood.
    D) HYPERGLYCEMIA and HYPOKALEMIA may occur. Monitor blood glucose and serum potassium levels. Monitor renal and liver function tests. Elevated BUN and liver enzyme levels have been noted.
    E) Six workers poisoned with a combination of dimethyltin and trimethyltin had urinary tin concentrations of 555 to 1600 mcg/L.
    F) Human tissue tin ranged from 0.2 to 0.6 mg/kg, with higher concentration in lung, which increases with age and tin oxide exposure.
    G) CT scan may be useful in the evaluation of patients suspected of having cerebral edema. Intracranial pressure monitoring may be useful in patients with cerebral edema. EEG may be abnormal in patients with organotin exposure. Monitor EKG for signs of hypokalemia. If hearing impairment is suspected, audiograms may be helpful in evaluation.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting.
    C) GASTRIC LAVAGE: Consider after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour). Protect airway by placement in the head down left lateral decubitus position or by endotracheal intubation. Control any seizures first.
    1) CONTRAINDICATIONS: Loss of airway protective reflexes or decreased level of consciousness in unintubated patients; following ingestion of corrosives; hydrocarbons (high aspiration potential); patients at risk of hemorrhage or gastrointestinal perforation; and trivial or non-toxic ingestion.
    D) Administration of activated charcoal is generally benign; it is recommended following ingestion of the organotin salts.
    1) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    E) BAL - was NOT an effective antidote in animals for trialkyltins, and therefore, SHOULD NOT BE EFFECTIVE for tetralkyltins. D-penicillamine did NOT cause an increased tin excretion when used in organotin poisoning.
    F) Cerebral edema may occur. See main document under TREATMENT, ORAL EXPOSURE for treatment recommendations.
    G) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    H) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    I) Respiratory depression or coma may occur. Ensure adequacy of respirations and oxygenation. Endotracheal intubation, assisted ventilation, and supplemental oxygenation could be necessary.
    J) Monitor EKG for signs of HYPOKALEMIA. Monitor blood glucose and serum potassium. Correct abnormalities as indicated.
    K) Monitor for the development of urinary retention and relieve with bladder catheterization if necessary.
    L) Follow-up should be arranged to evaluate and treat possible visual, hearing, neurological, and psychiatric sequelae.
    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.
    B) Organotin salts may cause pulmonary irritation of several days duration. Remove patient from exposure and observe for pulmonary irritation or pulmonary edema.
    C) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    D) SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).
    1) Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
    2) Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.
    E) Respiratory depression or coma may occur. Ensure adequacy of respirations and oxygenation. Endotracheal intubation, assisted ventilation, and supplemental oxygenation could be necessary.
    F) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    G) Monitor EKG for signs of HYPOKALEMIA. Monitor blood glucose and serum potassium. Correct abnormalities as indicated.
    H) Cerebral edema may occur. See main document under TREATMENT, INHALATION EXPOSURE for treatment recommendations.
    I) BAL - was NOT an effective antidote in animals for trialkyltins, and therefore, SHOULD NOT BE EFFECTIVE for tetralkyltins. D-penicillamine did NOT cause an increased tin excretion when used in organotin poisoning.
    J) Monitor for the development of urinary retention and relieve with bladder catheterization if necessary.
    K) Followup should be arranged to evaluate and treat possible visual, hearing, neurological, and psychiatric sequelae.
    0.4.4) EYE EXPOSURE
    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).
    B) Prolonged initial flushing and early ophthalmologic consultation may be advisable if severe irritation or corneal burns are present. Ophthalmologic consultation should also be obtained if visual sequelae develop.
    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).
    2) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    3) CHEMICAL BURNS - may occur. See main document under TREATMENT, DERMAL EXPOSURE for treatment recommendations.
    4) Organotin compounds are primary skin irritants and can be absorbed through intact skin, although the only serious poisonings to date have followed ingestion and inhalation. If systemic poisoning occurs following dermal exposure:
    a) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Range Of Toxicity

    A) The toxicity of most organotins is not well documented. The estimated toxic dose of triethyltin is 70 milligrams within 8 days. Triethyltin is estimated to be 10 times as toxic as diethyltin orally.
    B) Guinea pigs fed 50 ppm of acetoxytriphenylstannane in the died all died during the first 6 weeks. In rats given 50 ppm daily by stomach tube, 70% died of secondary infection in an average of 26.6 days. When fed in the diet, 300 ppm for 10 weeks was fatal.
    C) Rats given 5 to 25 mg/kg by the oral route over 170 days developed no symptoms. Guinea pigs fed 10 and 20 ppm of acetoxytriphenylstannane in the diet developed leukopenia, and increased water content of the brain and spinal cord was noted at the 20 ppm dose. Acetoxytriphenylstannane showed cumulative toxicity in this species.
    D) Rats fed 200 ppm in the diet for 10 weeks survived. Doses as low as 25 ppm were associated with reduced food intake, reduced growth, and decreased blood leukocytes in this species.

Clinical Effects

Summary Of Exposure

    A) Acetoxytriphenylstannane (triphenyltin acetate) is a trialkyl organotin compound. It is a colorless to white needle-like crystalline solid that is practically insoluble in water, and is used as a fungicide, algicide, and wood preservative. It can be absorbed systemically following ingestion, inhalation, and dermal contact, and is a skin irritant.
    1) Acetoxytriphenylstannane is available as a wettable powder and a technical product of at least 94 percent purity.
    2) Triphenyltin acetate has caused hepatic injury with irreversible hepatomegaly and elevated liver function tests with chronic occupational exposure. It also caused skin irritation with pruritus and erythema which developed 2 to 3 days after prolonged dermal contact with contaminated garments. Eye irritation has also occurred.
    a) Triphenyltin acetate may also cause blurred vision, headache, dizziness, loss of consciousness, malaise, visual disturbances, shortness of breath, epigastric pain, nausea, vomiting, and diarrhea. Glycosuria and hyperglycemia have been described.
    3) Because the group of ORGANOTIN compounds have a number of toxic effects IN COMMON, the following discussion deals with VARIOUS ORGANOTIN COMPOUNDS.

Heent

    3.4.1) SUMMARY
    A) Blurred vision, nystagmus, irritation, and photophobia have been described.
    B) Long-term sequelae of acute poisoning have included visual abnormalities.
    C) Tinnitus or deafness may occur, particularly following ingestion.
    D) Symptoms of trialkyl tin intoxication include nasal irritation.
    3.4.3) EYES
    A) BLURRED VISION - Onset of blurred vision occurred 24 hours after an ingestion of triphenyltin in an adult (Wu et al, 1990).
    B) NYSTAGMUS has been reported following ingestion of triphenyltin (Wu et al, 1990; Lin et al, 1998).
    C) IRRITATION - Eye irritation has occurred with occupational organotin exposure (ACGIH, 1986; Hathaway, 1996; (Sittig, 1991).
    1) Triphenyl tin is a severe irritant of the eye (HSDB , 2000). Acetoxytriphenylstannane causes eye irritation (HSDB , 2000).
    D) PHOTOPHOBIA may occur, particularly following ingestion (Sittig, 1985; Ellenhorn & Barceloux, 1988).
    E) SEQUELAE - Long-term sequelae of acute poisoning have included visual abnormalities (Ellenhorn & Barceloux, 1988).
    3.4.4) EARS
    A) DEAFNESS - Tinnitus or deafness may occur, particularly following ingestion (Sittig, 1985; Ellenhorn & Barceloux, 1988).
    3.4.5) NOSE
    A) IRRITATION - Symptoms of trialkyl tin intoxication include nasal irritation (Louria et al, 1972; Besser et al, 1987; Winship, 1988).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory tract irritation and cough have occurred with occupational organotin exposure. Systemic organotin poisoning has occurred following inhalation exposure. Respiratory depression may occur, particularly following ingestion. Symptoms of trialkyl tin intoxication include shortness of breath.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Respiratory tract irritation, and cough have occurred with occupational organotin exposure (ACGIH, 1991) Hathaway, 1996; (Sittig, 1991).
    B) SYSTEMIC DISEASE
    1) Systemic organotin poisoning has occurred following inhalation exposure (Hathaway, 1996; (Baselt, 1997).
    C) ACUTE RESPIRATORY INSUFFICIENCY
    1) Respiratory depression may occur, particularly following ingestion (Sittig, 1991; Ellenhorn & Barceloux, 1988).
    D) DYSPNEA
    1) Symptoms of trialkyl tin intoxication include shortness of breath (Louria et al, 1972; Besser et al, 1987; Winship, 1988).

Neurologic

    3.7.1) SUMMARY
    A) Encephalopathy, confusion, coma, sensorimotor polyneuropathy, headache, nausea, EEG changes, dizziness, vertigo, disorientation, psychosis, and weakness or flaccid paralysis of the limbs may occur, particularly following ingestion.
    B) Cerebral edema has been described following exposure to certain organotin compounds. Seizures and a diffuse sensation of pain may occur. Tremors may be noted.
    C) Long-term sequelae of acute poisoning have included paresthesias, headaches, visual abnormalities, aggressive behavior, memory deficits, and extrapyramidal hyperkinesis.
    3.7.2) CLINICAL EFFECTS
    A) TOXIC ENCEPHALOPATHY
    1) Confusion progressing to unconsciousness began approximately 12 days after a 23-year-old male ingested a molluscicidal agent, triphenyltin. He remained unconscious for about 1.5 months (Wu et al, 1990).
    2) Encephalopathy with involuntary hand movements, facial twitching, silly smile, crying, diplopia, bidirectional nystagmus, vertigo, and disorientation is reported (Lin et al, 1998).
    B) NEUROPATHY
    1) Delayed sensorimotor polyneuropathy due to axonal degeneration and demyelination developed in a 23-year-old male following an ingestion of triphenyltin (Wu et al, 1990).
    C) ELECTROENCEPHALOGRAM ABNORMAL
    1) Headache and nausea may follow mild exposures; EEG changes have been reported (Sittig, 1985).
    D) CLOUDED CONSCIOUSNESS
    1) Dizziness, vertigo, disorientation, psychosis, and weakness or flaccid paralysis of the limbs may occur, particularly following ingestion (Sittig, 1985; Ellenhorn & Barceloux, 1988).
    E) CEREBRAL EDEMA
    1) Cerebral edema has been described following exposure to certain organotin compounds (Hathaway, 1996).
    F) SEIZURE
    1) Seizures and a diffuse sensation of pain may occur (Ellenhorn & Barceloux, 1988). Tremors may be noted (Barnes & Stoner, 1959).
    G) SEQUELA
    1) Long-term sequelae of acute poisoning have included paresthesias, headaches, visual abnormalities, aggressive behavior, memory deficits, and extrapyramidal hyperkinesis (Ellenhorn & Barceloux, 1988).

Gastrointestinal

    3.8.1) SUMMARY
    A) Abdominal pain, diarrhea, retching, nausea, and vomiting have been reported after triphenyltin ingestion.
    B) Based on their other irritant properties, organotin compounds would be predicted to cause esophageal or gastrointestinal tract irritation or burns following ingestion.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) Abdominal pain, diarrhea, and vomiting have been reported after triphenyl tin ingestion (Wu et al, 1990).
    B) ABDOMINAL PAIN
    1) Abdominal pain, vomiting, nausea, and retching have occurred with organotin exposure (ACGIH, 1991) Hathaway, 1996; (Sittig, 1985; Ellenhorn & Barceloux, 1988).
    C) GASTROINTESTINAL IRRITATION
    1) Based on their other irritant properties, organotin compounds would be predicted to cause esophageal or gastrointestinal tract irritation or burns following ingestion.

Hepatic

    3.9.1) SUMMARY
    A) Hepatic necrosis and hepatomegaly have been described following exposure to certain organotin compounds. Laboratory abnormalities in organotin poisoning include elevated liver function tests.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) Hepatic necrosis and hepatomegaly have been described following exposure to certain organotin compounds (Hathaway, 1996). The development of chronic liver disease following a single acute exposure is reported in a single case (Mijatovic, 1972).
    B) LIVER ENZYMES ABNORMAL
    1) Laboratory abnormalities in organotin poisoning include elevated liver function tests (Ellenhorn & Barceloux, 1988; Lin et al, 1998).

Genitourinary

    3.10.1) SUMMARY
    A) Urinary retention or increased BUN may occur.
    B) Nephropathy has been reported.
    3.10.2) CLINICAL EFFECTS
    A) RETENTION OF URINE
    1) Urinary retention may occur, particularly following ingestion (Sittig, 1985; Ellenhorn & Barceloux, 1988).
    B) BLOOD UREA ABNORMAL
    1) Metabolic abnormalities included increased BUN (Klaassen et al, 1986).
    C) TOXIC NEPHROPATHY
    1) Nephropathy due to apparently reversible proximal tubular injury is reported in a series of three human exposures (Lin & Hsueh, 1993).

Hematologic

    3.13.1) SUMMARY
    A) Laboratory abnormalities in organotin poisoning include leukocytosis and leukopenia.
    3.13.2) CLINICAL EFFECTS
    A) LEUKOCYTOSIS
    1) Laboratory abnormalities in organotin poisoning include leukocytosis (Ellenhorn & Barceloux, 1988) and leukopenia (Lin et al, 1998).
    3.13.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    a) Leukopenia and lymphopenia have been reported in chronic rabbit studies (Dacasto et al, 1994b) and in rats (HSDB , 2000).

Dermatologic

    3.14.1) SUMMARY
    A) Organotin compounds are primary skin irritants and can be absorbed through intact skin. Skin lesions and itching occurred with occupational organotin exposure. Symptoms of trialkyl tin intoxication include possible skin burns, erythema, or dermatitis.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) Organotin compounds are primary skin irritants and can be absorbed through intact skin (ACGIH, 1991) Hathaway, 1996; (Sittig, 1991; Ellenhorn & Barceloux, 1988). Skin lesions and itching occurred with occupational organotin exposure (ACGIH, 1991) Hathaway, 1996; (Sittig, 1991).
    B) CHEMICAL BURN
    1) Symptoms of trialkyl tin intoxication include possible skin burns, erythema, or dermatitis (Louria et al, 1972; Besser et al, 1987; Winship, 1988).

Musculoskeletal

    3.15.1) SUMMARY
    A) Weakness or flaccid paralysis of the limbs may occur, particularly following ingestion.
    3.15.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) Weakness or flaccid paralysis of the limbs may occur, particularly following ingestion (Sittig, 1985; Ellenhorn & Barceloux, 1988).

Endocrine

    3.16.1) SUMMARY
    A) Metabolic abnormalities including increased blood sugar (due to centrally mediated depletion of catecholamines) may occur.
    3.16.2) CLINICAL EFFECTS
    A) HYPERGLYCEMIA
    1) Metabolic abnormalities included increased blood sugar (due to centrally mediated depletion of catecholamines) (Klaassen et al, 1986).

Reproductive

    3.20.1) SUMMARY
    A) Teratogenicity from tin itself was not observed in animal studies. Triphenyltin itself was not teratogenic in rats.
    1) Specific developmental abnormalities in the musculoskeletal system, post-implantation mortality, change in litter size, behavior and weaning index have been noted in the offspring of rats administered Acetoxytriphenylstannane.
    a) In one rat study, acetoxytriphenylstannane was NOT teratogenic to the offspring, although a dose-dependent weight reduction in weight gain was observed in females. Behavioral changes have been noted in the pups of female rats fed acetoxytriphenylstannane during gestation.
    B) Acetoxytriphenylstannane caused a decrease in ovulation and female fertility in rats
    C) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    D) Toxic effects on the testes, epididymis and sperm duct have been observed in rat studies. Marked testicular atrophy developed in rats fed 20 mg/kg/day of acetoxytriphenylstannane for 20 days.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) Teratogenicity from tin itself was not observed in animal studies (Winship, 1988). Acetoxytriphenylstannane was NOT teratogenic to the offspring of rats at doses where maternal toxicity was seen, although a dose-dependent reduction in weight gain was observed in females (HSDB , 2000; Giavini et al, 1980; Schardein, 1985).
    2) Acetoxytriphenyltin acetate was embryotoxic and fetotoxic, but not teratogenic, in rats at doses up to 12 mg/kg/day (days 7 to 17 of gestation), which were also maternally toxic (Noda et al, 1991).
    3) 20 mg/kg/day produced ovarian and fertility changes in the rat with gross reductions in ovarian weight (Newton & Hayes, 1968).
    4) Specific developmental abnormalities in the musculoskeletal system, post-implantation mortality, change in litter size, behavior and weaning index have been noted in the offspring of rats administered acetoxytriphenylstannane (RTECS , 2000; Lehotzky et al, 1982).
    5) Other organotins have been reported NOT to be teratogenic in experimental animals (Winship, 1988).
    3.20.3) EFFECTS IN PREGNANCY
    A) ANIMAL STUDIES
    1) Acetoxytriphenylstannane caused a decrease in ovulation and female fertility in rats (Newton & Hayes, 1968).
    a) Behavioral changes of transient nature were reported in the offspring of female rats receiving 6 mg/kg acetoxytriphenylstannane on days 7 to 15 of gestation (Lehotzky et al, 1982).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS900-95-8 (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
    3.21.2) SUMMARY/HUMAN
    A) At the time of this review, no studies were found on the possible carcinogenic activity of triphenyltin acetate in humans.
    3.21.4) ANIMAL STUDIES
    A) LACK OF EFFECT
    1) Carcinogenicity was not observed in animal studies (Winship, 1988).
    2) Triphenyltin hydroxide was not found to be carcinogenic in an NCI carcinogenesis bioassay (Sittig, 1985).
    3) Acetoxytriphenylstannane has been classed neoplastic by RTECS criteria in the mouse with the presence of liver tumors (RTECS , 2000). However, it was NOT tumorigenic when given to mice at the maximum tolerated dose for 18 months (HSDB , 2000).

Genotoxicity

    A) This compound induced an increase in micronuclei using in vitro and in vivo assays.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) The average blood tin concentration in normal individuals is 0.14 mg/L; some normal individuals do not have detectable tin in the blood.
    D) HYPERGLYCEMIA and HYPOKALEMIA may occur. Monitor blood glucose and serum potassium levels. Monitor renal and liver function tests. Elevated BUN and liver enzyme levels have been noted.
    E) Six workers poisoned with a combination of dimethyltin and trimethyltin had urinary tin concentrations of 555 to 1600 mcg/L.
    F) Human tissue tin ranged from 0.2 to 0.6 mg/kg, with higher concentration in lung, which increases with age and tin oxide exposure.
    G) CT scan may be useful in the evaluation of patients suspected of having cerebral edema. Intracranial pressure monitoring may be useful in patients with cerebral edema. EEG may be abnormal in patients with organotin exposure. Monitor EKG for signs of hypokalemia. If hearing impairment is suspected, audiograms may be helpful in evaluation.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) The average blood tin concentration in normal individuals is 0.14 mg/L; some normal individuals do not have detectable tin in the blood (Baselt, 1997).
    2) One worker who developed symptoms of malaise, headache, dizziness, and an enlarged liver while spraying acetoxytriphenylstannane had a tin blood level of 48 mcg/L and a urine tin level of 113 mcg/L on admission to hospital (HSDB , 2000).
    3) HYPERGLYCEMIA and HYPOKALEMIA may occur. Monitor blood glucose and serum potassium levels.
    4) Monitor renal and liver function tests. Elevated BUN and liver enzyme levels have been noted.
    5) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count and liver and kidney function tests is suggested for patients with significant exposure.
    4.1.3) URINE
    A) URINARY LEVELS
    1) Six workers poisoned with a combination of dimethyltin and trimethyltin had urinary tin concentrations of 555 to 1600 mcg/L (Baselt, 1997).
    B) URINALYSIS
    1) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring urinalysis is suggested for patients with significant exposure.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) If respiratory tract irritation is present, monitor arterial blood gases and chest x-ray.
    b) Human tissue tin ranged from 0.2 to 0.6 mg/kg, with higher concentration in lung, which increases with age and tin oxide exposure (Winship, 1988).
    c) CT scan may be useful in the evaluation of patients suspected of having cerebral edema.
    1) Intracranial pressure monitoring may be useful in patients with cerebral edema.
    d) Electroencephalogram may be abnormal in patients with organotin exposure.
    e) Monitor EKG for signs of hypokalemia.
    f) If hearing impairment is suspected, audiograms may be helpful in evaluation.
    g) If respiratory tract irritation is present, it may be useful to monitor pulmonary function tests.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) If respiratory tract irritation is present, monitor chest x-ray.

Treatment

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) Do NOT induce emesis.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) GASTRIC LAVAGE
    1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
    a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
    2) PRECAUTIONS:
    a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
    b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
    3) LAVAGE FLUID:
    a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
    b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
    c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
    4) COMPLICATIONS:
    a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
    b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
    5) CONTRAINDICATIONS:
    a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
    D) 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) IRRITATION SYMPTOM
    1) Some tin salts may be irritating or caustic. For these dilution should be done and emesis avoided unless significant ingestion presents risk of sufficient absorption to produce systemic toxicity.
    2) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    3) Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    B) CHELATION THERAPY
    1) BAL - (Dimercaprol)
    a) BAL - has been tried only in animal studies. It was an effective antidote against the general symptoms of dialkyltins, but did not prevent the biliary tract damage (Barnes & Stoner, 1958).
    b) BAL - was NOT an effective antidote in animals for trialkyltins, and therefore, SHOULD NOT BE EFFECTIVE for tetralkyltins (Aldridge & Cremer, 1955).
    2) D-penicillamine did NOT cause an increased tin excretion when used in organotin poisoning (Ellenhorn & Barceloux, 1988).
    C) CEREBRAL EDEMA
    1) CLINICAL IMPLICATIONS
    a) Cerebral edema and elevated intracranial pressure (ICP) may occur. Emergent management includes head elevation and administration of mannitol; hyperventilation should be performed if there is evidence of impending herniation.
    2) MONITORING
    a) Patients will usually require endotracheal intubation and mechanical ventilation. Monitor intracranial pressure, cerebral perfusion pressure and cerebral blood flow.
    3) TREATMENT
    a) Most information on the treatment of cerebral edema is derived from studies of traumatic brain injury.
    4) MANNITOL
    a) ADULT/PEDIATRIC DOSE: 0.25 to 1 gram/kilogram intravenously over 10 to 15 minutes (None Listed, 2000).
    b) AVAILABLE FORMS: Mannitol injection (5%, 10%, 15%, 20%, 25%).
    c) MAJOR ADVERSE REACTIONS: Congestive heart failure, hypernatremia, hyponatremia, hyperkalemia, renal failure, pulmonary edema, and allergic reactions.
    d) PRECAUTIONS: Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia. Do not add to whole blood for transfusions; enhanced neuromuscular blockade has occurred with tubocurarine. Keep serum osmolarity below 320 mOsm.
    e) MONITORING PARAMETERS: Renal function, urine output, fluid balance, serum potassium levels, serum osmolarity, and CVP.
    5) HYPERTONIC SALINE
    a) Preliminary studies suggest that hypertonic saline (7.5% saline/6% dextran) 100 ml reduced ICP more effectively than 200 mL of 20% mannitol in adults with elevated ICP after traumatic brain injury(Battison et al, 2005).
    6) ELEVATION
    a) Elevation of the head of the bed to approximately 30 degrees decreases ICP and improves cerebral perfusion pressure (Meixensberger et al, 1997; Schneider et al, 1993; Feldman et al, 1992).
    7) MECHANICAL DECOMPRESSION
    a) Early surgical decompression, ventriculostomy with CSF drainage, or craniectomy may be useful in patients with persistent elevation of ICP (Sahuquillo & Arikan, 2006; Sakai et al, 1998; Polin et al, 1997; Taylor et al, 2001). Most experience with these modalities has been in patients with traumatic brain injury.
    8) HYPERVENTILATION
    a) SUMMARY: Hyperventilation has been associated with adverse outcomes and should not be performed routinely (Muizelaar et al, 1991). It is indicated in patients who have clinical evidence of herniation or if there is intracranial hypertension refractory to sedation, paralysis, CSF drainage and osmotic diuretics (None Listed, 2000a).
    b) RECOMMENDATION:
    1) The PCO2 must be controlled in the range of 25 torr; further lowering of PCO2 may create undesirable effects secondary to local tissue hypoxia.
    2) End-tidal CO2 tension, correlated with an initial ABG measurement, provides a noninvasive means of monitoring PCO2 (Mackersie & Karagianes, 1990).
    3) Most authorities advise that hyperventilation should be considered a temporizing measure only; SUSTAINED hyperventilation should be avoided (Am Acad Neurol, 1997; Bullock et al, 1996; Kirkpatrick, 1997).
    D) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    E) AIRWAY MANAGEMENT
    1) Respiratory depression or coma may occur. Ensure adequacy of respirations and oxygenation. Endotracheal intubation, assisted ventilation, and supplemental oxygenation could be necessary.
    F) MONITORING OF PATIENT
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    3) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    4) Monitor EKG for signs of HYPOKALEMIA. Monitor blood glucose and serum potassium. Correct abnormalities as indicated.
    5) Monitor for the development of URINARY RETENTION and relieve with bladder catheterization if necessary.
    G) FOLLOW-UP VISIT
    1) Follow-up should be arranged to evaluate and treat possible visual, hearing, neurological, and psychiatric sequelae.

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.
    6.7.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) ORGANOTIN SALTS - may cause pulmonary irritation of several days duration. Remove patient from exposure and observe for pulmonary irritation or pulmonary edema.
    B) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    C) SEIZURE
    1) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    2) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    3) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    4) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).
    5) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    6) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
    D) AIRWAY MANAGEMENT
    1) Respiratory depression or coma may occur. Ensure adequacy of respirations and oxygenation. Endotracheal intubation, assisted ventilation, and supplemental oxygenation could be necessary.
    E) MONITORING OF PATIENT
    1) Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    2) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    3) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    4) Monitor EKG for signs of HYPOKALEMIA. Monitor blood glucose and serum potassium. Correct abnormalities as indicated.
    5) Monitor for the development of URINARY RETENTION and relieve with bladder catheterization if necessary.
    F) CEREBRAL EDEMA
    1) CLINICAL IMPLICATIONS
    a) Cerebral edema and elevated intracranial pressure (ICP) may occur. Emergent management includes head elevation and administration of mannitol; hyperventilation should be performed if there is evidence of impending herniation.
    2) MONITORING
    a) Patients will usually require endotracheal intubation and mechanical ventilation. Monitor intracranial pressure, cerebral perfusion pressure and cerebral blood flow.
    3) TREATMENT
    a) Most information on the treatment of cerebral edema is derived from studies of traumatic brain injury.
    4) MANNITOL
    a) ADULT/PEDIATRIC DOSE: 0.25 to 1 gram/kilogram intravenously over 10 to 15 minutes (None Listed, 2000).
    b) AVAILABLE FORMS: Mannitol injection (5%, 10%, 15%, 20%, 25%).
    c) MAJOR ADVERSE REACTIONS: Congestive heart failure, hypernatremia, hyponatremia, hyperkalemia, renal failure, pulmonary edema, and allergic reactions.
    d) PRECAUTIONS: Contraindicated in well-established anuria or impaired renal function not responding to a test dose, pulmonary edema, CHF, severe dehydration; caution in progressive oliguria and azotemia. Do not add to whole blood for transfusions; enhanced neuromuscular blockade has occurred with tubocurarine. Keep serum osmolarity below 320 mOsm.
    e) MONITORING PARAMETERS: Renal function, urine output, fluid balance, serum potassium levels, serum osmolarity, and CVP.
    5) HYPERTONIC SALINE
    a) Preliminary studies suggest that hypertonic saline (7.5% saline/6% dextran) 100 ml reduced ICP more effectively than 200 mL of 20% mannitol in adults with elevated ICP after traumatic brain injury(Battison et al, 2005).
    6) ELEVATION
    a) Elevation of the head of the bed to approximately 30 degrees decreases ICP and improves cerebral perfusion pressure (Meixensberger et al, 1997; Schneider et al, 1993; Feldman et al, 1992).
    7) MECHANICAL DECOMPRESSION
    a) Early surgical decompression, ventriculostomy with CSF drainage, or craniectomy may be useful in patients with persistent elevation of ICP (Sahuquillo & Arikan, 2006; Sakai et al, 1998; Polin et al, 1997; Taylor et al, 2001). Most experience with these modalities has been in patients with traumatic brain injury.
    8) HYPERVENTILATION
    a) SUMMARY: Hyperventilation has been associated with adverse outcomes and should not be performed routinely (Muizelaar et al, 1991). It is indicated in patients who have clinical evidence of herniation or if there is intracranial hypertension refractory to sedation, paralysis, CSF drainage and osmotic diuretics (None Listed, 2000a).
    b) RECOMMENDATION:
    1) The PCO2 must be controlled in the range of 25 torr; further lowering of PCO2 may create undesirable effects secondary to local tissue hypoxia.
    2) End-tidal CO2 tension, correlated with an initial ABG measurement, provides a noninvasive means of monitoring PCO2 (Mackersie & Karagianes, 1990).
    3) Most authorities advise that hyperventilation should be considered a temporizing measure only; SUSTAINED hyperventilation should be avoided (Am Acad Neurol, 1997; Bullock et al, 1996; Kirkpatrick, 1997).
    G) CHELATION THERAPY
    1) BAL - (Dimercaprol)
    a) BAL - has been tried only in animal studies. It was an effective antidote against the general symptoms of dialkyltins, but did not prevent the biliary tract damage (Barnes & Stoner, 1958).
    b) BAL - was NOT an effective antidote in animals for trialkyltins, and therefore, SHOULD NOT BE EFFECTIVE for tetralkyltins (Aldridge & Cremer, 1955).
    2) D-penicillamine did NOT cause an increased tin excretion when used in organotin poisoning (Ellenhorn & Barceloux, 1988).
    H) FOLLOW-UP VISIT
    1) Follow-up should be arranged to evaluate and treat possible visual, hearing, neurological, and psychiatric sequelae.
    I) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.8.2) TREATMENT
    A) IRRITATION SYMPTOM
    1) Organotin salts (especially dialkyl or trialkyltin compounds) have been known to produce eye irritation, photophobia, and visual disturbances.
    B) OPHTHALMIC EXAMINATION AND EVALUATION
    1) CONSULTATION - Prolonged initial flushing and early ophthalmologic consultation may be advisable if significant irritation or corneal burns are present.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

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).
    6.9.2) TREATMENT
    A) BURN
    1) Dibutyl and tributyltins have caused burns and dermatitis.
    2) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    3) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    4) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    5) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) IRRITATION SYMPTOM
    1) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    C) SKIN ABSORPTION
    1) Organotin compounds are primary skin irritants and can be absorbed through intact skin, although serious poisonings to date have generally followed ingestion and inhalation (ACGIH, 1991) Hathaway, 1996; (Sittig, 1991; Ellenhorn & Barceloux, 1988).
    2) Acute dermal exposure to acetoxytriphenylstannane resulted in dermatitis, edema, urticaria, hepatic dysfunction, and neurological abnormalities in a single case report (Colosio et al, 1991).
    3) If systemic poisoning occurs following dermal exposure:
    a) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    D) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) A number of chemicals produce abnormalities of the hematopoietic system, liver, and kidneys. Monitoring complete blood count, urinalysis, and liver and kidney function tests is suggested for patients with significant exposure.
    B) If respiratory tract irritation or respiratory depression is evident, monitor arterial blood gases, chest x-ray, and pulmonary function tests.
    C) The average blood tin concentration in normal individuals is 0.14 mg/L; some normal individuals do not have detectable tin in the blood.
    D) HYPERGLYCEMIA and HYPOKALEMIA may occur. Monitor blood glucose and serum potassium levels. Monitor renal and liver function tests. Elevated BUN and liver enzyme levels have been noted.
    E) Six workers poisoned with a combination of dimethyltin and trimethyltin had urinary tin concentrations of 555 to 1600 mcg/L.
    F) Human tissue tin ranged from 0.2 to 0.6 mg/kg, with higher concentration in lung, which increases with age and tin oxide exposure.
    G) CT scan may be useful in the evaluation of patients suspected of having cerebral edema. Intracranial pressure monitoring may be useful in patients with cerebral edema. EEG may be abnormal in patients with organotin exposure. Monitor EKG for signs of hypokalemia. If hearing impairment is suspected, audiograms may be helpful in evaluation.

Range Of Toxicity

Summary

    A) The toxicity of most organotins is not well documented. The estimated toxic dose of triethyltin is 70 milligrams within 8 days. Triethyltin is estimated to be 10 times as toxic as diethyltin orally.
    B) Guinea pigs fed 50 ppm of acetoxytriphenylstannane in the died all died during the first 6 weeks. In rats given 50 ppm daily by stomach tube, 70% died of secondary infection in an average of 26.6 days. When fed in the diet, 300 ppm for 10 weeks was fatal.
    C) Rats given 5 to 25 mg/kg by the oral route over 170 days developed no symptoms. Guinea pigs fed 10 and 20 ppm of acetoxytriphenylstannane in the diet developed leukopenia, and increased water content of the brain and spinal cord was noted at the 20 ppm dose. Acetoxytriphenylstannane showed cumulative toxicity in this species.
    D) Rats fed 200 ppm in the diet for 10 weeks survived. Doses as low as 25 ppm were associated with reduced food intake, reduced growth, and decreased blood leukocytes in this species.

Minimum Lethal Exposure

    A) ANIMAL DATA
    1) Guinea pigs fed 50 ppm of acetoxytriphenylstannane in the diet all died during the first 6 weeks (HSDB , 2000).
    2) In rats given 50 ppm daily by stomach tube, 70% died of secondary infection in an average of 26.6 days (HSDB , 2000). When fed in the diet, 300 ppm for 10 weeks was fatal (HSDB , 2000).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) The toxicity of most organotins is not well documented. The estimated toxic dose of triethyltin is 70 milligrams within 8 days (Barnes & Stoner, 1959). Triethyltin is estimated to be 10 times as toxic as diethyltin orally (Barnes & Stoner, 1959).
    2) Abdominal pain, diarrhea, and vomiting occurred several hours after an acute ingestion of triphenyltin in a 23-year-old male. On the day following the ingestion severe ataxia, dysmetria, nystagmus, and blurred vision were reported (Wu et al, 1990).
    a) Mental status changes developed 12 days after ingestion, progressing to coma which lasted for 1.5 months. A delayed sensorimotor polyneuropathy, which resolved with improved mental status, was also reported (Wu et al, 1990).
    B) ANIMAL DATA
    1) Rats given 5 to 25 mg/kg by the oral route over 170 days developed no symptoms (HSDB , 2000).
    2) Guinea pigs fed 10 and 20 ppm of acetoxytriphenylstannane in the diet developed leukopenia, and increased water content of the brain and spinal cord was noted at the 20 ppm dose (HSDB , 2000). Acetoxytriphenylstannane showed cumulative toxicity in this species (HSDB , 2000; Stoner & Heath, 1967).
    3) Rats fed 200 ppm in the diet for 10 weeks survived (HSDB , 2000). Doses as low as 25 ppm were associated with reduced food intake, reduced growth, and decreased blood leukocytes in this species (HSDB , 2000).
    4) In rats, the oral acute median lethal dose is 402 mg/kg. 200 mg/kg produced CNS and respiratory depression as well as injury to lung, liver, kidney, brain, and the intestinal mucosa (Attahiru et al, 1991).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2000
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) 7900 mcg/kg
    2) LD50- (ORAL)MOUSE:
    a) 81 mg/kg
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) 44 mg/kg
    4) LD50- (INTRAPERITONEAL)RAT:
    a) 8500 mcg/kg
    5) LD50- (ORAL)RAT:
    a) 125 mg/kg
    6) LD50- (SKIN)RAT:
    a) 450 mg/kg

Workplace Standards

    A) ACGIH TLV Values for CAS900-95-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS900-95-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS900-95-8 :
    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

    D) OSHA PEL Values for CAS900-95-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Physicochemical

Physical Characteristics

    A) White, crystalline solid (Lewis, 1996)
    B) White odorless crystals (Hayes & Laws, 1991)

Molecular Weight

    A) 409.07

References

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