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DIVINYL SULFONE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Divinyl sulfone is a compound with a high degree of sulfhydryl reactivity (La Rocca et al, 1975) which is used in the preparation of fabric dyes and may be liberated from them during the dyeing process (MacGregor et al, 1980).
    B) Divinyl sulfone has been suggested as a specific cellulose stain useful in histology (Salthouse et al, 1971), and has been used to activate Sepharose supports for the purification of various proteins (Ersson, 1977; DiCioccio et al, 1984; Lihme et al, 1986).
    C) Under certain conditions, divinyl sulfone may release oxides of sulfur (SOx) vapors (HSDB , 1992). SEE SULFUR DIOXIDE MANAGEMENT FOR MORE DETAILED INFORMATION.

Specific Substances

    A) No Synonyms were found in group or single elements
    1.2.1) MOLECULAR FORMULA
    1) C4-H6-02-S

Available Forms Sources

    A) USES
    1) Divinyl sulfone is a compound with a high degree of sulfhydryl reactivity (La Rocca et al, 1975) which is used in the preparation of fabric dyes and may be liberated from them during the dyeing process (MacGregor et al, 1980).
    2) It has also been used in the industrial formation of resins and was investigated during World War II for toxicity because of a chemical relationship to mustard gas (Grant, 1986).
    3) Divinyl sulfone has been suggested as a specific cellulose stain useful in histology (Salthouse et al, 1971), and has been used to activate Sepharose supports for the purification of various proteins (Ersson, 1977; DiCioccio et al, 1984; Lihme et al, 1986).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Very little information is available about the toxicity of divinyl sulfone. Exposed workers have had excessive lacrimation. Severe chemical burns may be seen after direct eye or skin contact.
    B) Renal impairment has been seen in experimental animals. Thermal decomposition or contact with acids may release oxides of sulfur vapors and produce mucous membrane irritation.
    C) Ingestion could cause gastrointestinal irritation and fluid shifts.
    0.2.4) HEENT
    A) Excessive lacrimation or severe corneal burns may occur.
    0.2.6) RESPIRATORY
    A) Inhalation could produce mucous membrane irritation.
    0.2.8) GASTROINTESTINAL
    A) Gastrointestinal irritation with possible fluid shifts could occur.
    0.2.10) GENITOURINARY
    A) Experimental animals have developed nephrotoxicity.
    0.2.12) FLUID-ELECTROLYTE
    A) Copius fluid losses into the peritoneal cavity from local irritation were noted in experimental animals following intraperitoneal injection.
    0.2.14) DERMATOLOGIC
    A) Direct skin contact can produce severe burns.
    0.2.17) METABOLISM
    A) In in vitro studies, divinyl sulfone had an inhibitory effect on pyruvate metabolism in rat liver and brain homogenates.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    B) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    0.2.21) CARCINOGENICITY
    A) At the time of this review, no data were available to assess the carcinogenic potential of this agent.
    0.2.22) OTHER
    A) Intraperitoneal injection of divinyl sulfone to rats produced irritation and copious edema of the peritoneal cavity.

Laboratory Monitoring

    A) Monitor renal function, urinary output, and serum electrolytes.
    B) Patients with significant inhalation exposure or respiratory tract irritation should have a baseline chest x-ray and arterial blood gases.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) 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.
    B) Do NOT induce emesis.
    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) 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) 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.
    F) Obtain baseline renal function tests and follow urinary output. Replace fluids and electrolytes as required.
    G) Neither hemodialysis nor hemoperfusion have been evaluated for efficacy in enhancing the elimination of divinyl sulfone. Hemodialysis could be useful to treat oliguric renal failure if it should occur.
    H) Treatment with n-acetylcysteine is not recommended.
    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) Obtain baseline renal function tests and follow urinary output. Replace fluids and electrolytes as required.
    C) Obtain baseline chest x-ray and arterial blood gases in patients with significant exposure to evolved oxides of sulfur vapors or respiratory tract irritation.
    D) Administer 100% supplemental humidified oxygen with assisted ventilation as required.
    E) Adrenergic bronchodilators or theophylline may be used for bronchospasm.
    F) 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.
    G) Treatment with n-acetylcysteine is not recommended.
    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.
    B) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    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) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Range Of Toxicity

    A) The minimum lethal human dose to this agent has not been delineated.
    B) The maximum tolerated human exposure to this agent has not been delineated.

Clinical Effects

Summary Of Exposure

    A) Very little information is available about the toxicity of divinyl sulfone. Exposed workers have had excessive lacrimation. Severe chemical burns may be seen after direct eye or skin contact.
    B) Renal impairment has been seen in experimental animals. Thermal decomposition or contact with acids may release oxides of sulfur vapors and produce mucous membrane irritation.
    C) Ingestion could cause gastrointestinal irritation and fluid shifts.

Heent

    3.4.1) SUMMARY
    A) Excessive lacrimation or severe corneal burns may occur.
    3.4.3) EYES
    A) LACRIMATION - Exposure to divinyl sulfone vapors has caused excessive lacrimation in workers (Grant, 1986).
    B) CORNEAL BURNS - Direct contact with divinyl sulfone has produced severe corneal burns in experimental animals (Grant, 1986).

Respiratory

    3.6.1) SUMMARY
    A) Inhalation could produce mucous membrane irritation.
    3.6.2) CLINICAL EFFECTS
    A) IRRITATION SYMPTOM
    1) Irritation of the respiratory tract following inhalation of vapors might be predicted based on the irritating properties of divinyl sulfone.

Gastrointestinal

    3.8.1) SUMMARY
    A) Gastrointestinal irritation with possible fluid shifts could occur.
    3.8.2) CLINICAL EFFECTS
    A) GASTRITIS
    1) Although gastrointestinal irritation has not been reported in humans or experimental animals, this effect might be predicted from the irritating properties of divinyl sulfone on skin, eyes, and the peritoneal cavity.

Genitourinary

    3.10.1) SUMMARY
    A) Experimental animals have developed nephrotoxicity.
    3.10.2) CLINICAL EFFECTS
    A) KIDNEY DISEASE
    1) ANIMAL STUDIES
    a) NEPHROTOXICITY - Rats injected intraperitoneally with sublethal doses of divinyl sulfone had decreased urinary output and elevated BUN, although there were no changes in urinary pH, and no glycosuria or proteinuria were found (La Rocca et al, 1975).
    b) The toxic effects of divinyl sulfone in molluscs and rats were felt to be due to impairment of renal function (La Rocca et al, 1975).

Dermatologic

    3.14.1) SUMMARY
    A) Direct skin contact can produce severe burns.
    3.14.2) CLINICAL EFFECTS
    A) CHEMICAL BURN
    1) DERMAL BURNS - Experimental animals have developed severe dermal burns after direct skin exposure to divinyl sulfone (Grant, 1986).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    B) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    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 CAS77-77-0 (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 data were available to assess the carcinogenic potential of this agent.
    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Genotoxicity

    A) Vinyl sulfone was found to be a chemical mutagen with induction of genotoxic effects at concentrations as low as 0.25 microgram/mL (Dearfield et al, 1991).
    B) At the time of this review, no data were available to assess the potential of this agent to produce DNA damage/repair or induce chromosome aberrations.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor renal function, urinary output, and serum electrolytes.
    B) Patients with significant inhalation exposure or respiratory tract irritation should have a baseline chest x-ray and arterial blood gases.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Baseline arterial blood gases should be obtained in patients with significant inhalation exposure to evolved oxides of sulfur vapors or signs of respiratory tract irritation.
    2) Based on animal experiments, patients ingesting divinyl sulfone could be at risk for severe gastrointestinal irritation with fluid shifts, and should have serum electrolytes and osmolality monitored.
    B) OTHER
    1) Patients with divinyl sulfone exposure should have baseline renal function tests.
    4.1.3) URINE
    A) URINALYSIS
    1) Follow urine output carefully in patients with significant divinyl sulfone exposure.

Radiographic Studies

    A) CHEST RADIOGRAPH
    1) Patients with significant inhalation exposure to evolved oxides of sulfur vapors or signs of respiratory tract irritation should have a baseline chest x-ray.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Monitor renal function, urinary output, and serum electrolytes.
    B) Patients with significant inhalation exposure or respiratory tract irritation should have a baseline chest x-ray and arterial blood gases.

Oral Exposure

    6.5.2) PREVENTION OF ABSORPTION
    A) 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).
    B) EMESIS/NOT RECOMMENDED
    1) Induced emesis SHOULD BE AVOIDED in divinyl sulfone ingestion.
    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/CATHARTIC
    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) 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.
    2) As fluid shifts might occur into an irritated gastrointestinal tract, hematocrit, serum electrolytes, and serum osmolality should be monitored.
    B) MONITORING OF PATIENT
    1) Obtain baseline renal function tests. Carefully follow urinary output.
    2) As fluid shifts might occur into an irritated gastrointestinal tract, hematocrit, serum electrolytes, and serum osmolality should be monitored.
    C) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Replace fluids and electrolytes as required. If there is a concomitant inhalation exposure, monitor carefully to avoid overhydration as pulmonary edema might result.
    D) EXPERIMENTAL THERAPY
    1) CYSTEINE - One in vitro experiment showed that divinyl sulfone inhibited the activity of malic dehydrogenase, and that this effect could be reversed by addition of cysteine (La Rocca et al, 1975).
    a) It is unknown whether this inhibition of malic dehydrogenase and reversal by cysteine occurs in vivo or what, if any, clinical implications it has. Treatment with n-acetylcysteine is therefore NOT RECOMMENDED.

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) AIRWAY MANAGEMENT
    1) Administer 100% supplemental humidified oxygen with assisted ventilation as required.
    B) MONITORING OF PATIENT
    1) Obtain baseline chest x-ray and arterial blood gases in patients with significant exposure to evolved oxides of sulfur vapors or respiratory tract irritation.
    2) Obtain baseline renal function tests. Carefully follow urinary output.
    C) 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).
    D) BRONCHOSPASM
    1) Bronchospasm could be treated with adrenergic bronchodilators or theophylline.
    E) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Replace fluids and electrolytes as required.
    F) EXPERIMENTAL THERAPY
    1) CYSTEINE - One in vitro experiment showed that divinyl sulfone inhibited the activity of malic dehydrogenase, and that this effect could be reversed by addition of cysteine (La Rocca et al, 1975).
    2) It is unknown whether this inhibition of malic dehydrogenase and reversal by cysteine occurs in vivo or what, if any, clinical implications it has. Treatment with n-acetylcysteine is therefore NOT RECOMMENDED.
    G) 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) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    B) 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) EXPERIMENTAL THERAPY
    1) SULFHYDRYL GROUPS - While experiments on an isolated enzyme system indicated that immediate flushing with agents with highly reactive sulfhydryl groups such as dimercaprol or mercaptoethanol might be beneficial (Grant, 1986), there is no clinical or in vivo experimental data supporting the use of this mode of treatment.
    2) CYSTEINE - One in vitro experiment showed that divinyl sulfone inhibited the activity of malic dehydrogenase, and that this effect could be reversed by addition of cysteine (La Rocca et al, 1975).
    a) It is unknown whether this inhibition of malic dehydrogenase and reversal by cysteine occurs in vivo or what, if any, clinical implications it has. Treatment with n-acetylcysteine is therefore NOT RECOMMENDED.
    B) BURN
    1) 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.
    2) 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).
    3) 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.
    4) 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.
    C) MONITORING OF PATIENT
    1) Obtain baseline renal function tests. Carefully follow urinary output.
    D) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Replace fluids and electrolytes as required.
    E) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) EXTRACORPOREAL ELIMINATION
    1) Neither hemodialysis nor hemoperfusion have been evaluated for efficacy in enhancing the elimination of divinyl sulfone. Hemodialysis could be useful to treat oliguric renal failure if it should occur.

Range Of Toxicity

Summary

    A) The minimum lethal human dose to this agent has not been delineated.
    B) The maximum tolerated human exposure to this agent has not been delineated.

Minimum Lethal Exposure

    A) GENERAL/SUMMARY
    1) The minimum human lethal exposure to divinyl sulfone has not been determined.
    B) ANIMAL DATA
    1) Rats have developed toxicity but survived with intraperitoneal injections of 2 to 2.5 milligrams/kilogram. The LD100 in rats was 3.5 milligrams/kilogram (La Rocca et al, 1975).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) The maximum tolerated human exposure to divinyl sulfone has not been determined.
    B) ANIMAL DATA
    1) Rats have developed toxicity but survived with intraperitoneal injections of 2 to 2.5 milligrams/kilogram (La Rocca et al, 1975).

Workplace Standards

    A) ACGIH TLV Values for CAS77-77-0 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS77-77-0 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS77-77-0 :
    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 CAS77-77-0 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 1992
    1) LD50- (SUBCUTANEOUS)MOUSE:
    a) 16 mg/kg
    2) LD50- (INTRAPERITONEAL)RAT:
    a) 3 mg/kg
    3) LD50- (ORAL)RAT:
    a) 32 mg/kg
    4) LD50- (SUBCUTANEOUS)RAT:
    a) 14 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Divinyl sulfone is a direct irritant of skin and mucous membranes due to its alkylating properties (Grant, 1986). In vitro, there is some evidence for inhibition of malic dehydrogenase and pyruvate metabolism, although this effect was not seen in an in vivo experiment (La Rocca et al, 1975).
    B) Divinyl sulfone produces direct impairment of renal function in experimental animals (La Rocca et al, 1975).

Physicochemical

Physical Characteristics

    A) Divinyl sulfone is a liquid (HSDB , 1992).

Molecular Weight

    A) 118.16 (HSDB , 1992)

References

General Bibliography

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