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SULFUR COMPOUNDS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) ELEMENTAL SULFUR is a dry powder available for dermatologic use in four forms: sublimed sulfur, washed sulfur, precipitated sulfur, and colloidal sulfur.
    B) OTHER SULFUR COMPOUNDS included in this management are sulfurated lime and sulfurated potash.

Specific Substances

    A) GENERAL TERMS
    1) aquilite
    2) asulfa-supra
    3) atomic sulfur
    4) azufre sublimado
    5) chloride of sulfur
    6) corosul d
    7) corosul s
    8) enxofre sublimado
    9) fleur de sonfre
    10) flowers of sulfur
    11) micowetsulf
    12) netzschwefel
    13) polsulkol
    14) rc-schwefel
    15) shreesul
    16) solfa
    17) sublimierter schwefel
    18) sufran
    19) sufran d
    20) sulfer sublimatum depuratum
    21) sulfex
    22) sulfospor
    23) sulfur atom
    24) sulfur chloride, mono
    25) sulfur colloid
    26) sulfur, molten
    27) sulfur, ointment
    28) sulfur, pharmaceutical
    29) sulikol
    30) sulphur chlorides
    31) sulphur, lump
    32) sulphur, powder
    33) sultaf
    34) super six
    35) svovl
    36) thion
    37) ultra sulfur
    38) zolvis
    SUBLIMED SULFUR
    1) azufre sublimado
    2) enxofre sublimado
    3) fleur de soufre
    4) flowers of sulfur
    5) sublimed sulphur
    6) sublimierter schwefel
    7) sulfur sublimatum depuratum
    8) sulphur sublimatum
    9) sulfur, sublimed
    10) CAS 7704-34-9
    WASHED SULFUR
    1) azufre lavado
    2) enxofre lavado
    3) gewaschener schwefel
    4) purified sulphur
    5) soufre lave
    6) sulfur lotum
    7) sulfur sublimatum lotum
    PRECIPITATED SULFUR
    1) milk of sulfur
    SULFURATED LIME
    1) calcium sulfuratum solutum
    2) calcium sulphide
    3) calx sulphurata
    4) sulphurated lime
    5) Vleminckx's solution
    6) CAS 8028-82-8 (solution)
    LIME SULFUR
    1) calcium polysulfides
    2) lime sulphur
    SULFURATED POTASH
    1) foie de soufre
    2) hepar sulfuris
    3) hepar Sulph
    4) kalii sulfidum
    5) liver of sulfur
    6) potassa sulphurata
    7) schwefelleber
    8) sulphurated potash
    9) CAS 39365-88-3

Available Forms Sources

    A) FORMS
    1) Elemental sulfur is a dry powder available for dermatologic use in four forms: sublimed sulfur, washed sulfur, precipitated sulfur, and colloidal sulfur.
    2) Sulfur Lime (Calcium polysulfide), sodium sulfide, ammonium sulfide and thioacetamide release hydrogen sulfide in contact with water or acids.
    3) Washed sulfur is made by washing sublimed sulfur with ammonia.
    4) Colloidal sulfur consists of minute particles of sulfur stabilized in an aqueous medium containing a colloid, such as egg albumin or gelatin.
    5) Sulfurated lime contains not less than 50% calcium sulfide. It is a mixture of sublimed sulfur, lime, and water, resulting in formation of calcium pentasulfide and calcium thiosulfate.
    6) Sulfurated potash is a mixture of potassium polysulphides and other potassium compounds, including sulfite and thiosulfate. It contains 42% to 45% sulfur, not less than 12.8% as sulfide (S Sweetman , 2001).
    7) White lotion USP contains 4% w/v sulfurated potash and 5% zinc sulfate.
    B) USES
    1) Sulfur is used in manufacturing sulfuric acid, as an insecticide and fungicide, in medicine as a laxative, antiseptic, and antiparasitic agent. Elemental sulfur is a dry powder available for dermatologic use.
    2) Sulphurated potash is used in homeopathic medicine (for the treatment of acne) where it is known as Hepar Sulph (S Sweetman , 2001).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) There are many types of sulfur compounds with a wide variety of clinical effects. Many are irritating to the skin, eyes, lungs, and GI tract.
    B) SUBACUTE EFFECTS of lime sulfur poisoning include: irritation of mucous membranes, respiratory tract irritation, rhinitis, and pulmonary edema are possible. Direct skin contact may produce pain and erythema. Ingestion can result in nausea, vomiting, diarrhea and central nervous system effects of giddiness, headache, vertigo, amnesia, confusion and unconsciousness. Other effects may include: tachycardia, cardiac dysrhythmias, sweating and weakness.
    C) ACUTE EFFECTS can result in sudden collapse and unconsciousness, and death from respiratory paralysis.
    D) PATHOPHYSIOLOGY - Sulfur Lime (Calcium polysulfide), sodium sulfide, ammonium sulfide and thioacetamide release hydrogen sulfide in contact with water or acids.
    E) In limited reports, ingestion of calcium polysulfide produced mucosal burns of the gastrointestinal tract and severe systemic effects which included mental status changes, coma, hypotension, dysrhythmias, hepatic and renal injury, rhabdomyolysis, metabolic acidosis and a fatal cardiac arrest. An intense odor of hydrogen sulfide (i.e., rotten eggs) was present in the gastric aspirate.
    0.2.6) RESPIRATORY
    A) Inhalation may result in shortness of breath, cough, tightness and burning of the chest, pulmonary edema, and even respiratory distress and failure. Pneumonia may occur after initial recovery.
    0.2.7) NEUROLOGIC
    A) Headache, vertigo, excitement or depression, loss of memory, and prostration may be observed. Tremors, seizures, coma, and death may result. Peripheral neuritis may follow after recovery.
    0.2.8) GASTROINTESTINAL
    A) Exposure may result in a hydrogen sulfide odor on the breath or in gastric aspirate, difficulty in swallowing, and redness of the tongue and pharynx. Lime sulfur is irritating on contact to the mucous membranes. Vomiting, abdominal pain, and diarrhea may occur.
    B) Mucosal burns of the esophagus and stomach have been reported following an ingestion of calcium polysulfide.
    0.2.9) HEPATIC
    A) Transient hepatic dysfunction was reported in a patient following an ingestion of calcium polysulfide.
    0.2.10) GENITOURINARY
    A) Urinary disturbances may occur. Renal dysfunction occurred in a patient following an ingestion of calcium polysulfide.
    0.2.11) ACID-BASE
    A) Metabolic acidosis may occur following exposures to high oral doses.
    0.2.14) DERMATOLOGIC
    A) Lime sulfur is irritating to the skin; burns have been reported following ingestion. Molten sulfur burns cause severe dermal injury.

Laboratory Monitoring

    A) No specific tests are indicated. Severe systemic effects have been reported following significant oral exposure.
    B) Monitor cardiac and respiratory function. Obtain a baseline ABG and repeat as indicated.
    C) In significant overdoses, renal and hepatic function should be observed.
    D) Obtain baseline electrolytes and acid/base balance in symptomatic patient and repeat as necessary.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) 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.
    C) 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.
    D) Patients should be monitored and treated symptomatically. Effects are variable depending on the route and amount of exposure. Hydrogen sulfide has been produced following ingestions of lime sulfur.
    E) Skin and eye irritation are possible following minor exposures. Moderate to severe effects can occur after large ingestions and result in gastrointestinal irritation and mucosal burns, as well as, cardiac, respiratory, and central nervous system effects.
    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.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) SULFUR - The acute oral toxic dose is estimated to be 10 to 15 grams in adults. Ingestions of 60 and 250 grams have been reported with recovery.
    B) SULFIDE SALTS - The alkali metal sulfide salts (sodium, potassium, calcium) are estimated to have a probable oral lethal dose of less than 5 mg/kg in humans.
    C) Fatalities have been reported following ingestion of calcium polysulfide.

Clinical Effects

Heent

    3.4.6) THROAT
    A) PHARYNGITIS - Exposure may result in a hydrogen sulfide odor on breath (i.e., rotten eggs), difficulty in swallowing and redness of the tongue and pharynx (Maddy & Edmiston, 1988). Lime sulfur is irritating on contact to the mucous membranes.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) ELECTROCARDIOGRAM ABNORMAL
    1) CASE REPORT
    a) ECG changes suggestive of myocardial infarction (acute ST elevations in anterior and lateral leads) were reported in a 23-year-old female 7 hours after ingesting half a cup of a fungicide containing 26% calcium polysulfide (562 mg/kg). Despite aggressive supportive care and resuscitation efforts, the patient died of a cardiac arrest 11 hours after exposure. There was no evidence of myocardial necrosis on autopsy (Horowitz et al, 1997).

Respiratory

    3.6.1) SUMMARY
    A) Inhalation may result in shortness of breath, cough, tightness and burning of the chest, pulmonary edema, and even respiratory distress and failure. Pneumonia may occur after initial recovery.
    3.6.2) CLINICAL EFFECTS
    A) COUGH
    1) Inhalation may result in shortness of breath, cough, tightness and burning in the chest (Maddy & Edmiston, 1988).
    B) ACUTE LUNG INJURY
    1) Pulmonary edema may occur.
    C) APNEA
    1) Respiratory distress and failure may develop.
    D) PNEUMONIA
    1) Pneumonia may follow after recovery.
    2) CASE REPORT
    a) A 30-year-old male developed Klebsiella pneumonia approximately 9 days after ingesting half a pint (estimated dose 891 mg/kg) of a fungicide containing 26% calcium polysulfide. The patient recovered following aggressive supportive care (Horowitz et al, 1997).

Neurologic

    3.7.1) SUMMARY
    A) Headache, vertigo, excitement or depression, loss of memory, and prostration may be observed. Tremors, seizures, coma, and death may result. Peripheral neuritis may follow after recovery.
    3.7.2) CLINICAL EFFECTS
    A) HEADACHE
    1) Headache has been reported (Maddy & Edmiston, 1988).
    B) DIZZINESS
    1) Vertigo has occurred.
    C) AMNESIA
    1) Memory loss has been reported.
    D) FATIGUE
    1) Prostration has developed.
    E) SEIZURE
    1) ANIMAL DATA - Tremors, seizures and death have been reported in animals (Greengard & Woolley, 1940).
    F) SECONDARY PERIPHERAL NEUROPATHY
    1) Peripheral neuritis may follow after recovery.
    G) COMA
    1) CASE REPORT
    a) A 23-year-old female was found comatose 30 minutes after ingesting half a cup of a fungicide containing 26% calcium polysulfide. Initial neurological findings were as follows: pupils were dilated to 6 mm and sluggish, flaccid without any response to painful stimuli. The patient died 11 hours after exposure of a cardiac arrest despite aggressive management (Horowitz et al, 1997).
    H) PSYCHOMOTOR AGITATION
    1) CASE REPORT
    a) Combativeness was reported in a 30-year-old male after being found by paramedics following ingestion of half a pint (estimated dose 891 mg/kg) of a fungicide containing 26% calcium polysulfide. The patient also had nonpurposeful movement and was unable to speak. Following aggressive supportive care the patient made a complete recovery with no permanent neurological deficits reported (Horowitz et al, 1997).

Gastrointestinal

    3.8.1) SUMMARY
    A) Exposure may result in a hydrogen sulfide odor on the breath or in gastric aspirate, difficulty in swallowing, and redness of the tongue and pharynx. Lime sulfur is irritating on contact to the mucous membranes. Vomiting, abdominal pain, and diarrhea may occur.
    B) Mucosal burns of the esophagus and stomach have been reported following an ingestion of calcium polysulfide.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA, VOMITING AND DIARRHEA
    1) Abdominal pain, nausea, vomiting and/or diarrhea may occur following toxic ingestions.
    B) VOMIT ODOR OFFENSIVE
    1) CASE REPORTS
    a) The odor of rotten eggs was present in the gastric aspirate (emesis and lavage fluid) in two patients following overdose of calcium polysulfide (fungicide product). In one case it was so intense that some healthcare personnel were overcome by the odor and had to refrain from care of that patient (Horowitz et al, 1997).
    C) BURN
    1) CASE REPORT
    a) A 30-year-old male developed mucosal burns of the esophagus and stomach following ingestion of a 26% calcium polysulfide solution (estimated dose 891 mg/kg). The patient was placed on bowel rest and upon follow-up the patient had an esophageal stricture and required dilatation (Horowitz et al, 1997).

Hepatic

    3.9.1) SUMMARY
    A) Transient hepatic dysfunction was reported in a patient following an ingestion of calcium polysulfide.
    3.9.2) CLINICAL EFFECTS
    A) ABNORMAL LIVER FUNCTION
    1) Elevated SGOT (1549 IU/L {peak}) and SGPT (2088 IU/L {peak}) were reported in a 30-year-old male who ingested half a pint of 26% calcium polysulfide solution (estimated dose 891 mg/kg). Levels peaked on hospital day 4, and bilirubin peaked on day 9 at 15.8 mg/dL. No permanent hepatic dysfunction was reported (Horowitz et al, 1997).

Genitourinary

    3.10.1) SUMMARY
    A) Urinary disturbances may occur. Renal dysfunction occurred in a patient following an ingestion of calcium polysulfide.
    3.10.2) CLINICAL EFFECTS
    A) MICTURITION FINDING
    1) Urinary disturbance may develop.
    B) ABNORMAL RENAL FUNCTION
    1) Elevated BUN (45 mg/dL) and creatinine (3.3 mg/dL) were reported, on hospital day 9, in a 30-year-old male who ingested half a pint of 26% calcium polysulfide solution (estimated dose 891 mg/kg) on hospital day 9. Renal function normalized with intravenous hydration only (Horowitz et al, 1997).

Acid-Base

    3.11.1) SUMMARY
    A) Metabolic acidosis may occur following exposures to high oral doses.
    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) CASE REPORTS
    a) Two patients developed metabolic acidosis following ingestion of a fungicide that contained 26% calcium polysulfide (i.e., fungicide). Both received aggressive decontamination and management. The first patient (a 23-year-old female) ingested approximately 562 mg/kg and died 11 hours after exposure from a cardiac arrest. The other patient was a 30-year-old male who recovered after ingesting 891 mg/kg (Horowitz et al, 1997).
    b) Metabolic acidosis with a high anion gap was reported in a 66-year-old woman who ingested 200 grams of sulfur over 2 days (Schwartz et al, 1986).
    c) Metabolic acidosis with a normal anion gap and hyperchloremia was described in a 57-year-old woman who ingested 250 grams of sulfur over 6 days (Blum & Coe, 1977).

Dermatologic

    3.14.1) SUMMARY
    A) Lime sulfur is irritating to the skin; burns have been reported following ingestion. Molten sulfur burns cause severe dermal injury.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) LIME SULFUR is irritating on contact to the skin.
    2) In concentrations above 15%, SULFUR is irritating to the skin. Prolonged application of less concentrated material may also cause irritation. Sulfur may cause progressive reddening, thickening, and scaling of the skin, with eventual erythroderma (FDA, 1982).
    3) Concentrations of 1 to 2% cause a keratoplastic effect, consisting of mild epidermal damage, followed by stimulation of keratin formation and epidermal thickening.
    a) Concentrations of 5 to 15% are keratolytic, causing peeling of the upper epidermis and stratum corneum (FDA, 1982).
    B) CHEMICAL BURN
    1) Molten sulfur burns cause severe dermal injury (Ungaro-Mancusi & Blackwell, 1983).
    2) Mucosal burns of the stomach and esophagus were reported in an adult following ingestion of a fungicide containing 26% calcium polysulfide (Horowitz et al, 1997). Esophageal stricture developed in this patient.

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7704-34-9 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    B) IARC Carcinogenicity Ratings for CAS8028-82-8 (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

Summary Of Exposure

    A) There are many types of sulfur compounds with a wide variety of clinical effects. Many are irritating to the skin, eyes, lungs, and GI tract.
    B) SUBACUTE EFFECTS of lime sulfur poisoning include: irritation of mucous membranes, respiratory tract irritation, rhinitis, and pulmonary edema are possible. Direct skin contact may produce pain and erythema. Ingestion can result in nausea, vomiting, diarrhea and central nervous system effects of giddiness, headache, vertigo, amnesia, confusion and unconsciousness. Other effects may include: tachycardia, cardiac dysrhythmias, sweating and weakness.
    C) ACUTE EFFECTS can result in sudden collapse and unconsciousness, and death from respiratory paralysis.
    D) PATHOPHYSIOLOGY - Sulfur Lime (Calcium polysulfide), sodium sulfide, ammonium sulfide and thioacetamide release hydrogen sulfide in contact with water or acids.
    E) In limited reports, ingestion of calcium polysulfide produced mucosal burns of the gastrointestinal tract and severe systemic effects which included mental status changes, coma, hypotension, dysrhythmias, hepatic and renal injury, rhabdomyolysis, metabolic acidosis and a fatal cardiac arrest. An intense odor of hydrogen sulfide (i.e., rotten eggs) was present in the gastric aspirate.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No specific tests are indicated. Severe systemic effects have been reported following significant oral exposure.
    B) Monitor cardiac and respiratory function. Obtain a baseline ABG and repeat as indicated.
    C) In significant overdoses, renal and hepatic function should be observed.
    D) Obtain baseline electrolytes and acid/base balance in symptomatic patient and repeat as necessary.
    4.1.2) SERUM/BLOOD
    A) In a limited number of case reports, severe systemic effects have been reported following ingestion of lime sulfur.
    1) Monitor neurological, cardiac and respiratory function following a significant ingestion. Obtain a baseline ABG and repeat as indicated.
    2) Monitor electrolytes and renal and hepatic function as indicated in symptomatic patients.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) No specific tests are indicated. Severe systemic effects have been reported following significant oral exposure.
    B) Monitor cardiac and respiratory function. Obtain a baseline ABG and repeat as indicated.
    C) In significant overdoses, renal and hepatic function should be observed.
    D) Obtain baseline electrolytes and acid/base balance in symptomatic patient and repeat as necessary.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/ NOT RECOMMENDED -
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) ACTIVATED CHARCOAL -
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS
    1) EMESIS: Ipecac-induced emesis is not recommended because of the potential for CNS depression and seizures.
    B) 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.
    C) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Treatment is symptomatic and supportive. Monitor cardiac and respiratory function following a significant ingestion. Obtain electrolyte and renal and hepatic function levels as indicated.
    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) ACIDOSIS
    1) Large doses of sulfur may produce metabolic acidosis (Blum & Coe, 1977; Schwartz et al, 1986).
    2) METABOLIC ACIDOSIS: Treat severe metabolic acidosis (pH less than 7.1) with sodium bicarbonate, 1 to 2 mEq/kg is a reasonable starting dose(Kraut & Madias, 2010). Monitor serum electrolytes and arterial or venous blood gases to guide further therapy.
    3) In patients with renal failure, hemodialysis may be required to correct electrolyte abnormalities.
    D) ABNORMAL BODY ODOR
    1) Hydrogen sulfide can be produced following normal decomposition of lime sulfur in the stomach. Provide adequate ventilation during care. Healthcare personnel have been overcome by the odor following two separate cases of lime sulfur ingestion (Horowitz et al, 1997). See the HYDROGEN SULFIDE management for further information as indicated.
    E) BURN
    1) SUMMARY - Mucosal burns of the esophagus and stomach have been reported following limited reports of oral exposure to lime sulfur (calcium polysulfide). Endoscopy may be indicated following significant ingestions.
    F) ENDOSCOPIC PROCEDURE
    1) SUMMARY: Obtain consultation concerning endoscopy as soon as possible and perform endoscopy within the first 24 hours when indicated.
    2) INDICATIONS: Most studies associating the presence or absence of gastrointestinal burns with signs and symptoms after caustic ingestion have involved primarily alkaline ingestions. Because acid ingestion may cause severe gastric injury with fewer associated initial signs and symptoms, endoscopic evaluation is recommended in any patient with a definite history of ingestion of a strong acid, even if asymptomatic.
    3) RISKS: Numerous large case series attest to the relative safety and utility of early endoscopy in the management of caustic ingestion.
    a) REFERENCES: Gaudreault et al, 1983; Symbas et al, 1983; Crain et al, 1984; (Schild, 1985; Moazam et al, 1987; Sugawa & Lucas, 1989; Previtera et al, 1990; Zargar et al, 1991; Vergauwen et al, 1991; Gorman et al, 1992; Nuutinen et al, 1994)
    4) The risk of perforation during endoscopy is minimized by (Zargar et al, 1991):
    a) Advancing across the cricopharynx under direct vision
    b) Gently advancing with minimal air insufflation
    c) Never retroverting or retroflexing the endoscope
    d) Using a pediatric flexible endoscope
    e) Using extreme caution in advancing beyond burn lesion areas
    f) Most authors recommend endoscopy within the first 24 hours of injury, not advancing the endoscope beyond areas of severe esophageal burns, and avoiding endoscopy during the subacute phase of healing when tissue slough increases the risk of perforation (5 to 15 days after ingestion) (Zargar et al, 1991).
    5) GRADING
    a) Several scales for grading caustic injury exist. The likelihood of complications such as strictures, obstruction, bleeding and perforation is related to the severity of the initial burn (Zargar et al, 1991):
    b) Grade 0 - Normal examination
    c) Grade 1 - Edema and hyperemia of the mucosa; strictures unlikely.
    d) Grade 2A - Friability, hemorrhages, erosions, blisters, whitish membranes, exudates and superficial ulcerations; strictures unlikely.
    e) Grade 2B - Grade 2A plus deep discreet or circumferential ulceration; strictures may develop.
    f) Grade 3A - Multiple ulcerations and small scattered areas of necrosis; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding may occur.
    g) Grade 3B - Extensive necrosis through visceral wall; strictures are common, complications such as perforation, fistula formation, or gastrointestinal bleeding are more likely than with 3A.
    6) FOLLOW UP - If burns are found, follow 10 to 20 days later with barium swallow or esophagram.
    G) CORTICOSTEROID
    1) CORROSIVE INGESTION/SUMMARY: The use of corticosteroids for the treatment of caustic ingestion is controversial. Most animal studies have involved alkali-induced injury (Haller & Bachman, 1964; Saedi et al, 1973). Most human studies have been retrospective and generally involve more alkali than acid-induced injury and small numbers of patients with documented second or third degree mucosal injury.
    2) FIRST DEGREE BURNS: These burns generally heal well and rarely result in stricture formation (Zargar et al, 1989; Howell et al, 1992). Corticosteroids are generally not beneficial in these patients (Howell et al, 1992).
    3) SECOND DEGREE BURNS: Some authors recommend corticosteroid treatment to prevent stricture formation in patients with a second degree, deep-partial thickness burn (Howell et al, 1992). However, no well controlled human study has documented efficacy. Corticosteroids are generally not beneficial in patients with a second degree, superficial-partial thickness burn (Caravati, 2004; Howell et al, 1992).
    4) THIRD DEGREE BURNS: Some authors have recommended steroids in this group as well (Howell et al, 1992). A high percentage of patients with third degree burns go on to develop strictures with or without corticosteroid therapy and the risk of infection and perforation may be increased by corticosteroid use. Most authors feel that the risk outweighs any potential benefit and routine use is not recommended (Boukthir et al, 2004; Oakes et al, 1982; Pelclova & Navratil, 2005).
    5) CONTRAINDICATIONS: Include active gastrointestinal bleeding and evidence of gastric or esophageal perforation. Corticosteroids are thought to be ineffective if initiated more than 48 hours after a burn (Howell, 1987).
    6) DOSE: Administer daily oral doses of 0.1 milligram/kilogram of dexamethasone or 1 to 2 milligrams/kilogram of prednisone. Continue therapy for a total of 3 weeks and then taper (Haller et al, 1971; Marshall, 1979). An alternative regimen in children is intravenous prednisolone 2 milligrams/kilogram/day followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks then tapered (Anderson et al, 1990).
    7) ANTIBIOTICS: Animal studies suggest that the addition of antibiotics can prevent the infectious complications associated with corticosteroid use in the setting of caustic burns. Antibiotics are recommended if corticosteroids are used or if perforation or infection is suspected. Agents that cover anaerobes and oral flora such as penicillin, ampicillin, or clindamycin are appropriate (Rosenberg et al, 1953).
    8) STUDIES
    a) ANIMAL
    1) Some animal studies have suggested that corticosteroid therapy may reduce the incidence of stricture formation after severe alkaline corrosive injury (Haller & Bachman, 1964; Saedi et al, 1973a).
    2) Animals treated with steroids and antibiotics appear to do better than animals treated with steroids alone (Haller & Bachman, 1964).
    3) Other studies have shown no evidence of reduced stricture formation in steroid treated animals (Reyes et al, 1974). An increased rate of esophageal perforation related to steroid treatment has been found in animal studies (Knox et al, 1967).
    b) HUMAN
    1) Most human studies have been retrospective and/or uncontrolled and generally involve small numbers of patients with documented second or third degree mucosal injury. No study has proven a reduced incidence of stricture formation from steroid use in human caustic ingestions (Haller et al, 1971; Hawkins et al, 1980; Yarington & Heatly, 1963; Adam & Brick, 1982).
    2) META ANALYSIS
    a) Howell et al (1992), analyzed reports concerning 361 patients with corrosive esophageal injury published in the English language literature since 1956 (10 retrospective and 3 prospective studies). No patients with first degree burns developed strictures. Of 228 patients with second or third degree burns treated with corticosteroids and antibiotics, 54 (24%) developed strictures. Of 25 patients with similar burn severity treated without steroids or antibiotics, 13 (52%) developed strictures (Howell et al, 1992).
    b) Another meta-analysis of 10 studies found that in patients with second degree esophageal burns from caustics, the overall rate of stricture formation was 14.8% in patients who received corticosteroids compared with 36% in patients who did not receive corticosteroids (LoVecchio et al, 1996).
    c) Another study combined results of 10 papers evaluating therapy for corrosive esophageal injury in humans published between January 1991 and June 2004. There were a total of 572 patients, all patients received corticosteroids in 6 studies, in 2 studies no patients received steroids, and in 2 studies, treatment with and without corticosteroids was compared. Of 109 patients with grade 2 esophageal burns who were treated with corticosteroids, 15 (13.8%) developed strictures, compared with 2 of 32 (6.3%) patients with second degree burns who did not receive steroids (Pelclova & Navratil, 2005).
    3) Smaller studies have questioned the value of steroids (Ferguson et al, 1989; Anderson et al, 1990), thus they should be used with caution.
    4) Ferguson et al (1989) retrospectively compared 10 patients who did not receive antibiotics or steroids with 31 patients who received both antibiotics and steroids in a study of caustic ingestion and found no difference in the incidence of esophageal stricture between the two groups (Ferguson et al, 1989).
    5) A randomized, controlled, prospective clinical trial involving 60 children with lye or acid induced esophageal injury did not find an effect of corticosteroids on the incidence of stricture formation (Anderson et al, 1990).
    a) These 60 children were among 131 patients who were managed and followed-up for ingestion of caustic material from 1971 through 1988; 88% of them were between 1 and 3 years old (Anderson et al, 1990).
    b) All patients underwent rigid esophagoscopy after being randomized to receive either no steroids or a course consisting initially of intravenous prednisolone (2 milligrams/kilogram per day) followed by 2.5 milligrams/kilogram/day of oral prednisone for a total of 3 weeks prior to tapering and discontinuation (Anderson et al, 1990).
    c) Six (19%), 15 (48%), and 10 (32%) of those in the treatment group had first, second and third degree esophageal burns, respectively. In contrast, 13 (45%), 5 (17%), and 11 (38%) of the control group had the same levels of injury (Anderson et al, 1990).
    d) Ten (32%) of those receiving steroids and 11 (38%) of the control group developed strictures. Four (13%) of those receiving steroids and 7 (24%) of the control group required esophageal replacement. All but 1 of the 21 children who developed strictures had severe circumferential burns on initial esophagoscopy (Anderson et al, 1990).
    e) Because of the small numbers of patients in this study, it lacked the power to reliably detect meaningful differences in outcome between the treatment groups (Anderson et al, 1990).
    6) ADVERSE EFFECTS
    a) The use of corticosteroids in the treatment of caustic ingestion in humans has been associated with gastric perforation (Cleveland et al, 1963) and fatal pulmonary embolism (Aceto et al, 1970).
    H) FOLLOW-UP VISIT
    1) Obtain a follow-up esophagram and upper GI series to evaluate presence or absence of secondary scarring and/or stricture formation about 2 to 4 weeks following ingestion.
    2) CASE REPORT - Two and half weeks after exposure, a 30-year-old male developed esophageal stricture requiring dilatation following ingestion of 26% calcium polysulfide (estimated dose: 891 mg/kg) (Horowitz et al, 1997).

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) ABNORMAL BODY ODOR
    1) Hydrogen sulfide can be produced following normal decomposition of lime sulfur in the stomach. Provide adequate ventilation during care. Healthcare personnel have been overcome by the odor following two separate cases of lime sulfur ingestion (Horowitz et al, 1997). See the HYDROGEN SULFIDE management for further information as indicated.
    B) 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).

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) Molten sulfur burns cooled on exposure to air forms a "cast." Debridement with a petrolatum-based antibiotic ointment leaves a protective emollient film between the sulfur and skin.
    2) Apply accepted standard of therapy for thermal or scald burns when sulfur cast separates.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) SPECIFIC AGENT
    1) SUBLIMED SULFUR - A 57-year-old woman was reported to ingest 250 grams of sublimed sulfur over 6 days. She presented with progressive lethargy and confusion.
    a) She was noted to have a metabolic acidosis with normal anion gap (pH 7.19, sodium 126 mEq/L, potassium 8.6 mEq/L, chloride 104 mEq/L, and CO2 12 mmol/L).
    b) She was treated with intravenous hydration, sodium bicarbonate, and enemas, and recovered rapidly and uneventfully within 72 hours (Blum & Coe, 1977).
    2) SUBLIMED SULFUR - A 66-year-old woman with end-stage renal failure ingested 200 grams of sublimed sulfur over 2 days. She presented with chest pain, delirium, agitation, and disorientation.
    a) High anion gap metabolic acidosis was present (pH 6.72, sodium 150 mEq/L, potassium 9.1 mEq/L, chloride 107 mEq/L, and CO2 2.3 mEq/L). Serum chemistries were corrected with sodium bicarbonate and dialysis, and her sensorium cleared (Schwartz et al, 1986).

Range Of Toxicity

Summary

    A) SULFUR - The acute oral toxic dose is estimated to be 10 to 15 grams in adults. Ingestions of 60 and 250 grams have been reported with recovery.
    B) SULFIDE SALTS - The alkali metal sulfide salts (sodium, potassium, calcium) are estimated to have a probable oral lethal dose of less than 5 mg/kg in humans.
    C) Fatalities have been reported following ingestion of calcium polysulfide.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) The purgative dose is 2 to 4 grams for adults (Hayes, 1982).

Minimum Lethal Exposure

    A) CASE REPORTS
    1) SPECIFIC SUBSTANCE
    a) CALCIUM POLYSULFIDE SOLUTION - A 22-year-old student died after ingestion of 400 mL of calcium polysulfide solution (Hayes, 1982).
    b) CALCIUM POLYSULFIDE (26%) SOLUTION - A 23-year-old female died 11 hours after ingesting half a cup of a fungicide containing 26% calcium polysulfide (562 mg/kg) (Horowitz et al, 1997).
    c) SULFIDE SALTS - The alkali metal sulfide salts (sodium, potassium, calcium) are estimated to have a probable oral lethal dose of less than 5 milligrams/kilogram in humans (Gosselin, 1984).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) SULFUR/NON-TOXIC DOSE - 500 to 750 milligrams daily of colloidal sulfur produced no toxic effects when given to adult volunteers for 10 days (Greengard & Woolley, 1940).
    2) SULFUR/TOXIC DOSE - The acute oral toxic dose of sulfur has been estimated at 10 to 15 grams in adults (Deichmann & Gerarde, 1969) Council on Pharmacy and Chemistry, 1955).
    B) CASE REPORTS
    1) SULFUR/TOXIC-
    a) Ingestion of 250 grams of sulfur over 6 days produced acidosis and recovery in a 57-year-old woman (Blum & Coe, 1977).
    b) In one adult male, 60 grams of sulfur was ingested within 24 hours, which produced toxicity and complete recovery (Hodge et al, 1951).
    2) CALCIUM POLYSULFIDE (26%) SOLUTION-
    a) A 30-year-old male survived an ingestion of half a pint (estimated dose 891 mg/kg) of a fungicide containing 26% calcium polysulfide. Following aggressive supportive care the patient made a complete recovery with no permanent neurological deficits reported. Esophageal stricture was found after initial recovery (Horowitz et al, 1997).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) GENERAL
    a) NORMAL LEVELS - The normal serum sulfate is 0.5 to 1.5 milliequivalents/liter.
    b) TOXIC LEVELS -
    1) In a patient with metabolic acidosis secondary to sublimed sulfur ingestion, the serum sulfate was 2.3 milliequivalents/liter (Blum & Coe, 1977).
    2) In another case of sublimed sulfur-induced acidosis, the serum sulfate was 24.6 milliequivalents/liter (Schwartz et al, 1986).

Workplace Standards

    A) ACGIH TLV Values for CAS7704-34-9 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) ACGIH TLV Values for CAS8028-82-8 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    C) NIOSH REL and IDLH Values for CAS7704-34-9 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    D) NIOSH REL and IDLH Values for CAS8028-82-8 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    E) Carcinogenicity Ratings for CAS7704-34-9 :
    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

    F) Carcinogenicity Ratings for CAS8028-82-8 :
    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

    G) OSHA PEL Values for CAS7704-34-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

    H) OSHA PEL Values for CAS8028-82-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) SULFUR

Pharmacology Toxicology

Pharmacologic Mechanism

    A) In ruminants it is changed partly to hydrogen sulfide. Ingestion may cause hydrogen sulfide production due to bacteria in the colon.
    B) Sulfur has a keratolytic action when applied to the skin, secondary to the interaction of sulfur with cysteine present in keratinocytes. Sulfur is broken down to form hydrogen sulfide on the skin.
    1) When applied at high concentrations, the hydrogen sulfide breaks down keratin and causes dissolution of the stratum corneum (Lin et al, 1988).

Toxicologic Mechanism

    A) In limited case reports lime sulfur was able to produce severe systemic effects (i.e., coma, myocardial infarction, cardiac arrest, confusion, agitation rhabdomyolysis, and transient renal and hepatic dysfunction) following ingestion of a fungicide containing 26% calcium polysulfide (Horowitz et al, 1997).
    1) SUBACUTE poisoning can produce irritation to eyes, skin and respiratory tract. Neurological effects can include: giddiness, headache, confusion and amnesia. Pulmonary edema with dyspnea may occur. The following gastrointestinal effects have been reported: nausea, vomiting, and diarrhea (HSDB , 2001).
    2) ACUTE poisoning can result in sudden collapse and unconsciousness; death may occur from respiratory paralysis; cardiac dysrhythmias may be present. Recovery is generally slow (HSDB , 2001).

Physicochemical

Physical Characteristics

    A) LIME SULFUR: deep orange malodorous liquid
    B) SUBLIMED SULFUR: fine yellow, crystalline powder with a faint odor and taste
    C) WASHED SULFUR: fine odorless, tasteless, yellow crystalline powder
    D) PRECIPITATED SULFUR: fine, yellowish-white, amorphous, odorless powder with a smooth texture
    E) SULFURATED POTASH: greenish-yellow fragments with an odor of hydrogen sulfide

Molecular Weight

    A) Elemental sulfur: 32.07

Animal Toxicology

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) Steers fed excessive sodium sulfate had excess sulfide production in the rumen and developed polioencephalomalacia (Gould et al, 1991).

References

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