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HYDROGEN SULFIDE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Hydrogen sulfide is a flammable, heavier-than-air, colorless gas with a strong, offensive sulfur or "rotten eggs" odor and a sweetish taste. Because it rapidly paralyzes olfactory nerve endings in high concentrations, odor is not a dependable means of detecting this gas. It is commonly found in the presence of degrading protein waste and accumulates in confined spaces and low-lying areas. It is a leading cause of sudden death in the workplace. Natural gas containing hydrogen sulfide is termed "sour gas".

Specific Substances

    1) Dihydrogen monosulfide
    2) Dihydrogen sulfide
    3) Hydrogen sulphide
    4) Hydrosulfide
    5) Sulfur hydride
    6) Hydrogen sulfuric acid
    7) Hydrosulfuric acid
    8) Sulfureted hydrogen
    9) Molecular Formula: H2S
    10) CAS 7783-06-4
    11) CARBON OXIDE SULFIDE (COS)
    12) CARBON OXYSULFIDE (COS)
    13) CARBONYL SULFIDE (OCS)
    14) CARBONYL SULFIDE (SCO)
    15) H2S (MOLECULAR FORMULA) (HYDROGEN SULFIDE)
    16) HYDROGEN SULFIDE, LIQUEFIED
    17) OXYCARBON SULFIDE (COS)
    18) PHOSPHORUS PENTASULFIDE (FREE OF YELLOW OR WHITE PHOSPHORUS)
    1.2.1) MOLECULAR FORMULA
    1) H2-S

Available Forms Sources

    A) FORMS
    1) Hydrogen sulfide is a gas that is heavier than air and has an unpleasant odor of rotten eggs. It is detectable by odor at concentrations as low as 0.05 ppm.
    2) Hydrogen sulfide is a liquid at high pressures and low temperatures, and is shipped as the liquefied material under its own vapor pressure (AAR, 1996).
    3) Hydrogen sulfide is available commercially in a technical grade of 98.5 percent purity and a purified grade of 99.5 percent minimum purity (Lewis, 1993).
    B) SOURCES
    1) DETERGENT SUICIDE: Several suicides have been reported in Japan and the United States in individuals who combined household chemicals containing a sulfur component and an acid, resulting in the development of hydrogen sulfide gas. Mixing of these chemicals occurred in enclosed spaces (ie, a vehicle with rolled up windows or a bathroom), and the individuals would place signs on the outside of the window or door warning of toxic fumes contained within the enclosed space. In Japan, bath sulfur was typically mixed with an acidic toilet bowl cleaner, and in the United States the sulfur component used was an insecticide (Poulsen, 2009; Truscott, 2008)
    2) Natural sources include subterranean emissions (e.g., caves, wells, coal pits, springs), volcanoes (up to levels of 1:4000), and bacterial decomposition of sulfur in soil and the gastrointestinal tract (Ellenhorn, 1997; Sollmann, 1957). Emissions may be increased after water levels rise.
    3) Hydrogen sulfide is released spontaneously from decomposing sulfur compounds. It is also produced by bacterial action on sewage effluents containing sulfur compounds when oxygen has been consumed by excessive organic loading of surface water ("sewer gas").
    4) Poisonings have occurred in or near processing and storage tanks of liquid manure that are widely used to dispose of large volumes of livestock wastes (Morse et al, 1981; Osbern & Crapo, 1981). Agitation of the manure is important in creating an acute, severely toxic environment (Donham et al, 1982).
    5) Hydrogen sulfide may be generated from decomposing protein in the holds of fishing vessels (Glass et al, 1980; Dalgaard et al, 1972).
    6) Hydrogen sulfide is present in well-head gas found in natural gas in concentrations of up to 22% (220,000 ppm) where inhaling one breath can be immediately fatal (Kurt, 1992).
    7) Hydrogen sulfide is released during wood pulp production and paper and paperboard production and recycling (Kauppinen et al, 1997).
    8) Water reclamation workers may be exposed to hydrogen sulfide and tanker drivers may have more significant exposure than other workers in this field (Glass, 1990).
    9) Data from the United States Bureau of Labor Statistics show that hydrogen sulfide was responsible for 52 out of 43,950 fatal occupational injuries in the period from 1993 to 1999. Most exposures occurred in an enclosed space. The waste management (24%) and oil and natural gas (18%) industries were most often involved. Exposure was immediately fatal in 45 workers (87%) and there were 9 episodes (21%) with more than one death, some of whom were killed while attempting to rescue co-workers (Hendrickson et al, 2004).
    C) USES
    1) Hydrogen sulfide is used or encountered in farming (usually as agricultural disinfectants), brewing, tanning, glue making, rubber vulcanizing, metal recovery processes, heavy water production (for nuclear reactors), in oil ("sour crude" refinery) and gas exploration and processing, in rayon or artificial silk manufacture, lithography and photoengraving, fur-dressing and felt-making plants, abattoirs, fertilizer cookers, beet sugar factories, analytical chemistry, and dye production (Beck et al, 1981; Sittig, 1991; Grant, 1993; ACGIH, 1992).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Hydrogen sulfide is a highly toxic, colorless gas. It is denser than air with a rotten egg odor. Hydrogen sulfide is produced naturally by biological degradation of sulfur-containing products (eg, fish, sewage, and manure) and produced as a byproduct in many industrial processes (ie, paper mills, heavy-water production, petroleum refineries, tanneries, mines, carbon disulfide production, and hot asphalt fumes). It can often be found naturally in sulfur hot springs, volcanoes, and underground deposits of natural gas.
    B) TOXICOLOGY: It interrupts oxidative phosphorylation by inhibition of cytochrome oxidase a3. By inhibiting oxidative phosphorylation, hydrogen sulfide effectively causes cellular asphyxia.
    C) EPIDEMIOLOGY: Hydrogen sulfide exposure is uncommon; however, with severe exposure manifestations are life-threatening.
    D) WITH POISONING/EXPOSURE
    1) EXPOSURE: Hydrogen sulfide exposure occurs primarily by inhalation, but can also cause dermal and ocular injury. Suspect hydrogen sulfide toxicity in anyone found unconscious, in a confined space with an odor of rotten eggs present. Darkening of jewelry or silver coins in the vicinity of the victim should also heighten suspicion for hydrogen sulfide exposure.
    2) MILD TO MODERATE TOXICITY: In mild to moderate exposures, hydrogen sulfide is primarily an irritant causing upper-airway irritation, conjunctivitis, corneal injury, dermatitis, pharyngitis, pneumonitis, and pulmonary edema (which can be life-threatening). It can also manifest as headache, nausea, vomiting, chest pain, shortness of breath, weakness, dizziness, disequilibrium, keratoconjunctivitis, corneal ulceration and rarely irreversible corneal scarring.
    3) SEVERE TOXICITY: Severe exposure manifests as central nervous system depression, seizures, coma, hemoptysis, myocardial ischemia, dysrhythmias, acute lung injury, and death. Central nervous system depression is usually rapid and profound. While recovery may be complete in patients rapidly removed from exposure, permanent sequelae (eg, dementia, memory failure, delirium, ataxia, tremor, muscle rigidity) may result from prolonged hypoxia.
    0.2.20) REPRODUCTIVE
    A) Spontaneous abortions have occurred after exposure to life-threatening concentrations.
    0.2.21) CARCINOGENICITY
    A) In Rotorua, New Zealand (an active geothermal zone where hydrogen sulfide is released to the atmosphere), cancer deaths were not related to the extent of hydrogen sulfide exposure and there was no overall excess mortality found.

Laboratory Monitoring

    A) Specific laboratory studies for confirming hydrogen sulfide exposure are not readily available in most clinical laboratories and are often not clinically useful.
    B) Monitor serum electrolytes, BUN, creatinine, glucose, CBC, CPK, urinalysis, and ECG.
    C) Monitor vital signs, pulse oximetry and/or arterial blood gases and chest radiograph in patients with respiratory signs or symptoms.
    D) In the acutely ill patient, blood gas analysis may demonstrate metabolic acidosis, and elevated mixed venous oxygen measurement. Lactate is also usually elevated.
    E) Hydrogen sulfide can also be measured in the environment by many emergency response teams using electrochemical sensors.
    F) Brain CT may reveal white matter demyelination and degeneration of the globus pallidus in patients with severe poisoning.
    G) Monitor methemoglobin levels if nitrite antidotes are administered.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) For mild to moderate toxicity, remove the patient from the exposure and administer oxygen. Symptomatic and supportive care is the mainstay of treatment. Treat ocular injury with normal saline irrigation and perform an ocular exam (including visual acuity and slit lamp). Treat dermal injury by removing clothing and performing copious soap and water decontamination.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Severe toxicity usually manifests as CNS depression. Patients should be immediately removed from the offending environment, aggressive airway management including intubation, oxygen supplementation and crystalloid/pressor support should ensue. For patients with severe poisoning who are already receiving good supportive care, consider the administration of sodium nitrite. DOSE: Sodium Nitrite: Adult: 300 mg of 3% sodium nitrite (10 mL of a 3% solution) administered over 2.5 to 5 minutes; Pediatric: 0.12 to 0.33 mL/kg. There are anecdotal reports suggesting hyperbaric oxygen treatment may be useful if provided immediately after exposure. Hyperbaric oxygen therapy and nitrite therapy should only be instituted after maximum supportive measures have been instituted for severely ill patients, as there is no rigorous human evidence supporting either treatment.
    C) DECONTAMINATION
    1) PREHOSPITAL: Maximum personal protective gear (self-contained breathing apparatus) should be utilized for rescuers removing the victim from the toxic environment (would-be rescuers entering a contaminated environment often become victims). Administer high flow oxygen, and assist ventilation with a bag-valve-mask or perform endotracheal intubation, if necessary.
    2) HOSPITAL: Minimal off-gassing usually occurs in the hospital environment after the patient has been removed from the exposure. Administer high-flow oxygen. Irrigate eyes if there is evidence of irritation. Wash skin if there is evidence of irritation.
    D) AIRWAY MANAGEMENT
    1) Early endotracheal intubation and mechanical ventilation with high oxygen concentrations is recommended in patients with mental status depression or respiratory distress.
    E) ANTIDOTE
    1) Animal studies suggest that inducing methemoglobinemia reduces hydrogen sulfide toxicity, as hydrogen sulfide has a greater affinity for methemoglobin than for cytochrome oxidase. There are no clinical studies in human as hydrogen sulfide poisoning is rare. For patients with severe poisoning who are already receiving aggressive supportive care. Consider administration of sodium nitrite (Adult: 300 mg of 3% sodium nitrite (10 mL of a 3% solution) administered over 2.5 to 5 minutes; Pediatric: 0.12 to 0.33 mL/kg). Be aware that nitrites can induce hypotension and hypoxia and excessive methemoglobin formation can worsen tissue hypoxia in an unstable patient. There are anecdotal reports suggesting that hyperbaric oxygen treatment may be beneficial if provided immediately after exposure. Hyperbaric oxygen therapy and nitrite therapy should only be instituted after maximum supportive measures have been instituted for severely ill patients.
    F) PATIENT DISPOSITION
    1) HOME CRITERIA: All significant exposures should be sent to a hospital.
    2) OBSERVATION CRITERIA: Patients who are minimally symptomatic may be observed until resolution of symptoms in a healthcare facility.
    3) ADMISSION CRITERIA: Any severely ill patient should be admitted to an intensive care unit.
    4) CONSULT CRITERIA: Consult a medical toxicologist or a poison center for any severely poisoned patient. Data are controversial regarding hyperbaric therapy; however, if a hyperbaric center is readily available, contact a hyperbaric specialist to consult on a patient with severe poisoning. Consult an ophthalmologist for patients with keratoconjunctivitis or corneal ulceration.
    G) PITFALLS
    1) At high concentrations the ability to perceive the odor of hydrogen sulfide is rapidly lost because of olfactory nerve paralysis; this may be misinterpreted as dissolution of the gas. Rescuers should wear personal protective equipment (self-contained breathing apparatus) as they often become victims when they attempt to rescue other victims in environments with high concentrations of hydrogen sulfide. Victims often fall due to rapid loss of consciousness, evaluate for traumatic injuries. Hydrogen sulfide is an irritant; therefore, evaluate exposed patients for ocular or dermal injury.
    H) TOXICOKINETICS
    1) In severe cases, onset is rapid, duration depends upon continued exposure and environmental concentration. Hydrogen sulfide is oxidized to thiosulfate and polysulfides.
    I) DIFFERENTIAL DIAGNOSIS
    1) Cyanide, and other mitochondrial poisons.
    0.4.3) INHALATION EXPOSURE
    A) Immediately move the patient to fresh air and administer 100% oxygen. Prevent self-exposure and possible death by wearing a self-contained breathing apparatus to rescue the victim.
    B) 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.
    C) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    D) NITRITE THERAPY: IV sodium nitrite may be beneficial by forming sulfmethemoglobin, thus removing sulfide from combination in tissue. Do NOT use sodium thiosulfate. The antidotal efficacy of nitrite therapy is controversial; it should be considered in patients with severe symptoms who present soon after exposure.
    1) SODIUM NITRITE: Adult: 10 mL (300 mg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute; Child (with normal hemoglobin concentration): 0.2 mL/kg (6 mg/kg) of a 3% solution IV at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg).
    2) Repeat one-half of initial sodium nitrite dose one-half hour later if there is inadequate clinical response. Calculate pediatric doses precisely to avoid potentially life-threatening methemoglobinemia. Use with caution if carbon monoxide poisoning is also suspected. Monitor blood pressure carefully. Reduce nitrite administration rate if hypotension occurs.
    E) 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.
    0.4.5) 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) Concentrations of 50 to 100 ppm are associated with mild toxicity manifesting as respiratory tract irritation while concentrations greater than 500 ppm are usually associated with the loss of consciousness and death.
    B) At an airborne concentration of 0.05 ppm, hydrogen sulfide produces a characteristic odor of rotten eggs. The distinctive rotten egg odor cannot be detected at concentrations above 150 ppm.
    C) Exposure to greater than 500 ppm results in severe toxicity and death. Respiratory paralysis and death may be noted within 30 to 60 minutes. At 800 to 1000 ppm, death may be nearly immediate after 1 or more breaths.

Clinical Effects

Summary Of Exposure

    A) USES: Hydrogen sulfide is a highly toxic, colorless gas. It is denser than air with a rotten egg odor. Hydrogen sulfide is produced naturally by biological degradation of sulfur-containing products (eg, fish, sewage, and manure) and produced as a byproduct in many industrial processes (ie, paper mills, heavy-water production, petroleum refineries, tanneries, mines, carbon disulfide production, and hot asphalt fumes). It can often be found naturally in sulfur hot springs, volcanoes, and underground deposits of natural gas.
    B) TOXICOLOGY: It interrupts oxidative phosphorylation by inhibition of cytochrome oxidase a3. By inhibiting oxidative phosphorylation, hydrogen sulfide effectively causes cellular asphyxia.
    C) EPIDEMIOLOGY: Hydrogen sulfide exposure is uncommon; however, with severe exposure manifestations are life-threatening.
    D) WITH POISONING/EXPOSURE
    1) EXPOSURE: Hydrogen sulfide exposure occurs primarily by inhalation, but can also cause dermal and ocular injury. Suspect hydrogen sulfide toxicity in anyone found unconscious, in a confined space with an odor of rotten eggs present. Darkening of jewelry or silver coins in the vicinity of the victim should also heighten suspicion for hydrogen sulfide exposure.
    2) MILD TO MODERATE TOXICITY: In mild to moderate exposures, hydrogen sulfide is primarily an irritant causing upper-airway irritation, conjunctivitis, corneal injury, dermatitis, pharyngitis, pneumonitis, and pulmonary edema (which can be life-threatening). It can also manifest as headache, nausea, vomiting, chest pain, shortness of breath, weakness, dizziness, disequilibrium, keratoconjunctivitis, corneal ulceration and rarely irreversible corneal scarring.
    3) SEVERE TOXICITY: Severe exposure manifests as central nervous system depression, seizures, coma, hemoptysis, myocardial ischemia, dysrhythmias, acute lung injury, and death. Central nervous system depression is usually rapid and profound. While recovery may be complete in patients rapidly removed from exposure, permanent sequelae (eg, dementia, memory failure, delirium, ataxia, tremor, muscle rigidity) may result from prolonged hypoxia.

Vital Signs

    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) Fever may be a presenting sign in patients with seizures following acute exposure (Christia-Lotter et al, 2007; Gerasimon et al, 2007; Snyder et al, 1995; Schneider et al, 1998).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Hypotension or hypertension have occurred (Yalamanchili & Smith, 2008; Christia-Lotter et al, 2007; Gerasimon et al, 2007).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) Tachycardia or bradycardia may be seen (Christia-Lotter et al, 2007; Gerasimon et al, 2007).

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) ABNORMAL FUNDUS: The fundus of the eye had an abnormal appearance in a patient who had an acute exposure and subsequent keratitis epithelialis. The retinal veins seemed turgescent on the first day following poisoning. Moderate papilledema occurred after 2 days with a few retinal hemorrhages. The corneas returned to normal after five days (Grant, 1993).
    2) IRRITATION: Finnish residents exposed to hydrogen sulfide and other sulfur compounds in an area with Kraft process pulp mills complained of eye irritation (Haahtela et al, 1992; Marttila et al, 1994; Marttila et al, 1995).
    3) CONJUNCTIVITIS: Hydrogen sulfide is very irritating to the eyes causing painful conjunctivitis and corneal abrasions (ATSDR, 1998; Snyder et al, 1995). Injection of the conjunctivae, seeing colored halos ("gas eyes") (Done, 1979; ACGIH, 1992; Lewis, 1996) ocular pain, and blepharospasm may be noted following exposure to 150 ppm to 300 ppm.
    a) "Spinners eye" can occur in viscose manufacturing workers from hydrogen sulfide emissions in the viscose fiber spinning process (Beauchamp, 1984; Vanhoorne et al, 1995).
    b) Recovery from eye exposure to low concentrations is usually spontaneous over 24 to 72 hours (Grant, 1993).
    c) Exposure to 2100 mg/m(3) for 4 minutes in rats resulted in ocular irritation and exfoliation of ocular cells, with more exfoliation occurring at hydrogen sulfide exposures of 560 mg/m(3) for 4 hours (Lefebvre et al, 1991).
    4) MYOSIS: Bilateral myosis has been reported in a man following a massive inhalation of hydrogen sulfide. He died due to anoxic brain injury and massive myocardial necrosis less than 24 hours after admission to ICU (Christia-Lotter et al, 2007).
    5) PHOTOPHOBIA: It may occur as well as scratchy irritated eyes with burning and tearing (ATSDR, 1998; Grant, 1993).
    6) KERATOCONJUNCTIVITIS: A brief spurt of concentrated gas (50 ppm to 60 ppm) into the eyes may induce an intense keratoconjunctivitis (ATSDR, 1998; Grant, 1993).
    3.4.5) NOSE
    A) WITH POISONING/EXPOSURE
    1) OLFACTORY FATIGUE: Hydrogen sulfide can be detected at concentrations of 0.025 ppm by its characteristic and offensive odor of rotten eggs. Olfactory fatigue may occur after 2 to 15 minutes of exposure at 100 ppm. Olfactory fatigue occurs more rapidly at higher concentrations (Audeau et al, 1985).
    a) Recovery of smell is slow, depends on the extent of exposure, and may require weeks to months.
    2) IRRITATION: Finnish residents exposed to hydrogen sulfide and other sulfur compounds in an area with Kraft process pulp wills complained of nasal irritation (Haahtela et al, 1992; Marttila et al, 1994; Marttila et al, 1995).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension can occur with severe poisoning (Christia-Lotter et al, 2007; Gunn & Wong, 2001; ATSDR, 1998).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) An elevated blood pressure has been reported in patients exposed to hydrogen sulfide (Yalamanchili & Smith, 2008; Gerasimon et al, 2007; Audeau et al, 1985).
    b) CASE REPORT: An elevated blood pressure of 150/100 mmHg was reported on examination of a patient exposed to hydrogen sulfide. Within a few hours the blood pressure had returned to normal (120/80 mmHg) without treatment (Audeau et al, 1985).
    C) CONDUCTION DISORDER OF THE HEART
    1) WITH POISONING/EXPOSURE
    a) Tachycardia, bradycardia, and cardiac dysrhythmias have been reported (Yalamanchili & Smith, 2008; Nikkanen & Burns, 2004; Peters, 1981; Ravizza et al, 1982; Hoidal et al, 1986; Gregorakos et al, 1995). Tachycardia is a common effect following severe acute exposures (Christia-Lotter et al, 2007; Gerasimon et al, 2007; Gunn & Wong, 2001; ATSDR, 1998; Snyder et al, 1995; Schneider et al, 1998). There are also at least two reports of myocardial involvement, one of them with persistent atrial fibrillation (Simson & Simpson, 1971). These usually involve major exposures where hypoxia and lactic acidosis have occurred.
    D) MYOCARDIAL INFARCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Subendocardial infarction was reported in a 33-year-old man who simultaneously presented with emotional behavioral changes following exposure to 50 to 400 ppm hydrogen sulfide in the workplace (Vathenen et al, 1988).
    b) One patient died of a myocardial infarction 2 months after having acute hydrogen sulfide poisoning (Gregorakos et al, 1995).
    E) MYOCARDIAL NECROSIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Following a massive inhalation of hydrogen sulfide, a 22-year-old man presented with a Glasgow coma scale score of 7, prolonged seizures, and severe dyspnea. In the ICU, he had bilateral myosis, tachycardia, hypotension, and hyperthermia at 38 degrees C. Laboratory results showed elevated total CPK and normal troponin level. ECG and ultrasound revealed severe posterolateral hypokinesis of the heart. Less than 24 hours after admission to ICU, he died with acute respiratory distress complicated by severe hemodynamic insufficiency due to myocardial necrosis. Autopsy showed an anoxic/ischemic brain injury with edema, large areas of acidophilic necrosis in the heart, without contraction bands, and aspiration pneumonia(Christia-Lotter et al, 2007).
    F) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) Cardiac arrest may develop abruptly after high level exposure (Tanaka et al, 1999).
    b) CASE REPORT: A 34-year-old sewer worker was pulled from 20 feet below street level after approximately 45 minutes of hydrogen sulfide exposure (levels estimated greater than 1000 ppm). Upon arrival to the hospital, he was unresponsive, hypertensive, and tachycardic with a respiratory acidosis and pulmonary edema that progressed to acute lung injury. Supportive treatment along with sodium nitrite therapy was initiated, but the patient's status continued to decline. On hospital day 2 he was found in ventricular fibrillation; despite resuscitation efforts, the patient died 30 minutes later (Yalamanchili & Smith, 2008).
    c) CASE REPORT: A 24-year-old oil well worker was found by emergency medical services unresponsive and in cardiac arrest after an explosion at work. He was taken to a local emergency department after resuscitation and intubation. At this time, a strong odor of rotten eggs, consistent with hydrogen sulfide exposure, was noted. Laboratory results revealed an acute uncompensated metabolic acidosis (pH 7.25, PCO2 40 mm Hg, PO2 332 mmHg, bicarbonate 14 mmol/L) and elevated troponin (0.27 ng/mL), suggesting myocardial ischemia. An ECG revealed sinus tachycardia. He was transported to an ICU after stabilization and decontamination. Following supportive care, laboratory results revealed improvement in the metabolic acidosis, pH of 7.43, bicarbonate of 22 mmol/L, lactate of 1.2 mmol/L, and troponin of 1.1 ng/mL. He was placed in a hyperbaric oxygen chamber 1 hour after arrival to the ICU (10 hours postexposure) and remained there for 2 hours. During therapy, he developed sinus bradycardia (HR, 40 to 60 beats/min) and hypotension, treated with a bolus of norepinephrine. Approximately 14 hours after the initial exposure, he underwent therapeutic hypothermia for 24 hours to treat his cardiac arrest. His condition improved gradually and he was discharged after 5 days of hospitalization. After discharge, he experienced dysarthria, tunnel vision, numbness of his right arm, chronic headaches, and residual cognitive deficits, including poor working memory and a mild expressive aphasia (Asif & Exline, 2012).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOTENSION
    a) Rats administered sulfide injections of 120 mg/kg experienced hypotension (blood pressure decreasing by 43.6 +/- 4.0 mmHg from baseline) which returned to baseline within 15 minutes of the injection (Baldelli et al, 1993).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) The action of hydrogen sulfide is chiefly on the respiration with hyperpnea occurring at dilutions of 1:1500 followed by hypocapnia and apnea. With 1:500, there is immediate respiratory paralysis due to irritation of the carotid sinus (Sollmann, 1957; ACGIH, 1992). Neurogenic apnea or asphyxia is a cause of death in severe acute exposures.
    b) Exposure to 800 ppm to 1000 ppm can be fatal in 30 minutes or less, producing respiratory arrest (Lewis, 1996).
    c) Respiratory arrest is common in high concentration exposures (Gunn & Wong, 2001; Tanaka et al, 1999; ATSDR, 1998).
    B) ACUTE LUNG INJURY
    1) WITH POISONING/EXPOSURE
    a) Acute lung injury/ARDS may develop after significant exposure (Yalamanchili & Smith, 2008; Gerasimon et al, 2007; Nikkanen & Burns, 2004; Nam et al, 2004; Gunn & Wong, 2001; ATSDR, 1998; Tanaka et al, 1999; Schneider et al, 1998; Tvedt et al, 1991; Gregorakos et al, 1995; Osbern & Crapo, 1981; Ravizza et al, 1982; Whitcraft et al, 1985).
    b) ARDS may occur after prolonged exposure to hydrogen sulfide at concentrations greater than 250 ppm or acutely after exposures to concentrations between 750 ppm and 1000 ppm (Milby & Baselt, 1999).
    c) In a review of 3 case series of hydrogen sulfide poisoning in 523 patients, ARDS occurred in 4% to 16% of cases (Milby & Baselt, 1999).
    d) CASE REPORT: A 36-year-old man was found unconscious with no spontaneous respirations after exposure to hydrogen sulfide gas while cleaning a 50,000 gallon tank containing degrading eggs. A chest radiograph showed mild pulmonary edema; however, he did not experience any late or long-term sequelae from his acute lung injury (Gerasimon et al, 2007).
    e) CASE REPORT: A 46-year-old man, with a history of bronchial asthma, hypertension, and diabetes mellitus, was exposed to hydrogen sulfide fumes and presented 4 days later with worsening shortness of breath, dry cough, and noisy breathing. Despite treatment with oral steroids, theophylline, co-amoxiclav, and nebulized salbutamol and ipratropium bromide, his condition worsened over the next 3 days and he became very dyspneic, with an oxygen saturation on air of 88%. Despite further treatment with IV ceftriaxone, IV magnesium sulfate, oral potassium, frequent nebulizations, his condition continued to worsen, requiring non-invasive continuous positive airway pressure support and IV methylprednisolone. He gradually improved and was weaned off the ventilator 7 days after admission. On day 5, he was discharged with a diagnosis of late chemical pneumonitis and hypoxic cardiac ischemia (Shivanthan et al, 2013).
    C) BRONCHITIS
    1) WITH POISONING/EXPOSURE
    a) The irritant nature of hydrogen sulfide may produce acute bronchitis, but in the absence of reactive airways disease syndrome it is not associated with chronic disease (Lewis, 1996; ACGIH, 1992).
    b) CASE REPORT: A 63-year-old male died from acute hemorrhagic bronchitis secondary to use of a sulfuric acid drain cleaner which released hydrogen sulfide gas (Odera, 1975).
    c) Bronchial hyperresponsiveness has been reported in oil and gas workers rendered unconscious following hydrogen sulfide exposure (Hessel et al, 1997).
    d) Bronchial erythema and irritation was noted on bronchoscopy in three patients with hydrogen sulfide poisoning (Tanaka et al, 1999).
    D) PNEUMONITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Subacute exposure in a 30-year-old male resulted in interstitial pneumonitis with dyspnea, chest tightness, and hemoptysis 3 weeks after hydrogen sulfide gas exposure. Five months later the patient was asymptomatic except for residual exertional dyspnea and blood parameters were normal, but lung volumes and carbon monoxide diffusing capacity were still decreased (Parra et al, 1991).
    E) PULMONARY FUNCTION STUDIES ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) Sewer workers exposed to hydrogen sulfide had decreased lung function manifested as decreased FEV1/FVC on pulmonary function testing (Richardson, 1995).
    b) Pulmonary function generally improves over time but may not return to normal (Gunn & Wong, 2001).
    F) IRRITATION SYMPTOM
    1) WITH POISONING/EXPOSURE
    a) Finnish residents in an area with Kraft process pulp mills which release hydrogen sulfide and other sulfur compounds complained of coughing, pharyngeal irritation, breathlessness, and an increased incidence of respiratory infections (Partti-Pellinen et al, 1996; Marttila et al, 1995; Marttila et al, 1994; Haahtela et al, 1992).
    G) BRONCHOSPASM
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 40-year-old man presented with bronchospasm immediately after occupational exposure to hydrogen sulfide. Following treatment with nebulized salbutamol and ipratropium bromide along with IV hydrocortisone, his symptoms resolved. The patient's lab and imaging results remained normal and he was discharged 3 days after exposure with no further complications (Shivanthan et al, 2013).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) CNS depression occurs with depressed respiration (Christia-Lotter et al, 2007; Nikkanen & Burns, 2004; Peters, 1981).
    b) Inhalation exposure to 500 ppm for 30 minutes may produce headache, sweating, vertigo, seizures, irritability, somnolence, weakness, amnesia, malaise, confusion, delirium, hallucinations, nystagmus, unconsciousness, and coma (Audeau et al, 1985; Peters, 1981; Smith & Gosselin, 1979; Stine et al, 1976).
    c) A phenomenon referred to as "knock down", an abrupt, brief loss of consciousness, occurs with exposure to very high concentrations of hydrogen sulfide, ranging from 750 ppm to 1000 ppm (Milby & Baselt, 1999; Gabbay et al, 2001).
    d) Following a massive inhalation of hydrogen sulfide, a 22-year-old man presented with a Glasgow coma scale score of 7, prolonged seizures, and severe dyspnea. In the ICU, he had bilateral myosis, tachycardia, hypotension, and hyperthermia at 38 degrees Celsius. Laboratory results showed elevated total CPK and normal troponin level. ECG and ultrasound revealed severe posterolateral hypokinesis of the cardiac muscle. Less than 24 hours after admission to ICU, he died with acute respiratory distress complicated by severe hemodynamic insufficiency due to myocardial necrosis. Autopsy showed cerebral edema and anoxic brain injury (Christia-Lotter et al, 2007).
    e) CASE REPORT: A 36-year-old man was found unconscious with no spontaneous respirations after exposure to hydrogen sulfide gas while cleaning a 50,000 gallon tank containing degrading eggs. He did not receive nitrite or hyperbaric oxygen therapies since he arrived to the hospital outside the therapeutic window of effectiveness and had good tissue oxygenation. A neurologic exam revealed spontaneous decerebrate posturing and up-going toes bilaterally. On day 2, a brain MRI with diffusion-weighted imaging revealed areas of restricted diffusion in the left superior cerebral hemisphere and in the left basal ganglia and thalamus, consistent with an anoxic brain injury. Following supportive care and intensive neuro-rehabilitation, he slowly improved over the next several months (Gerasimon et al, 2007).
    f) CASE REPORT: Following inhalational exposure to hydrogen sulfide from the water of a thermal spring, a 25-year-old woman was found dead in a hotel room located next to the spring. Her autopsy revealed diffuse edema and pulmonary congestion. Her postmortem blood concentrations showed 0.68 mg/L of sulfide and 0.21 mmol/L of thiosulfate. A 26-year-old man in the same hotel room was found unconscious in bed. On presentation to a healthcare facility, he had a Glasgow Coma scale score of 5/15, a respiratory rate of 28 breaths/min, a blood pressure of 116/85 mmHg, a pulse of 135 beats/min, and a peripheral oxygen saturation of 74%. Blood gas analysis showed pH 7.09, PO2 52 mmHg, PCO2 72 mmHg; bicarbonate and lactate concentrations were normal. An ECG revealed sinus tachycardia. A chest x-ray showed pulmonary edema. His liver enzymes were mildly elevated. Following supportive care, his symptoms gradually improved and he was discharged home on day 3 (Daldal et al, 2010).
    g) CASE REPORT: A 36-year-old man, with a history of epilepsy, presented unconscious with cyanosis, labored-breathing, bronchospasms, and generalized muscle twitching within 1 hour of exposure to hydrogen sulfide. He had 3 generalized tonic-clonic seizures within a 30-minute period. Despite supportive care, including treatment with nebulized salbutamol and ipratropium, benzodiazepines, a single dose of IV hydrocortisone, and antidote sodium nitrite (treated within 15 minutes of admission), he developed recurrent seizures, deepening unconsciousness, and decerebrate posturing. Following further treatment with parenteral barbiturates, phenytoin sodium, and sodium valproate, he regained consciousness and was extubated by day 3; however, he developed truncal ataxia and dysarthria while also complaining of recent, mild left-sided hearing impairment. He continued to use phenytoin monotherapy and his symptoms gradually improved over the next 2 weeks. On day 20, he was discharged with residual mild-dysarthria, mild ataxia, as well as retrograde amnesia of events (Shivanthan et al, 2013)
    B) TOXIC ENCEPHALOPATHY
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Subacute encephalopathy with ataxia, choreoathetosis, and dystonia were described in a 20-month-old child after low level chronic exposure to hydrogen sulfide (Gaitonde et al, 1987). Brain CT scan demonstrated abnormalities of the basal ganglia and surrounding white matter. Other causes were not ruled out. Similar sequelae have been described after cyanide and carbon monoxide poisoning.
    b) CASE REPORT: Chronic exposure (20 years) via drinking water with hydrogen sulfide levels of 1.2 mg/L (EPA allowable limit of 0.05 mg/L) resulted in chronic encephalopathy associated with peroneal sensory neuropathy in a 43-year-old male. Discontinuing consumption of the contaminated water resulted in significant clinical improvement (Callender, 1993).
    C) SEQUELA
    1) WITH POISONING/EXPOSURE
    a) Permanent neurological sequelae (memory and motor function most commonly affected) have been reported following acute toxic exposures, likely secondary to hypoxic injury. Sequelae among survivors of acute toxic episodes include amnesia, cognitive impairment, intention tremor, rigidity, neurasthenia, disturbance of equilibrium or more serious brainstem and cortical damage (Ahlborg, 1951; Aufdermaur & Tonz, 1970; Hurwitz & Taylor, 1954; Kemper, 1966; McCabe & Clayton, 1952; Poda, 1966; Zeyer, 1955; Schneider et al, 1998; Hall & Rumack, 1997; Snyder et al, 1995; Tvedt et al, 1991; Kilburn, 1993; Wasch et al, 1989). However, complete recovery may occur following prompt resuscitation (Kleinfeld et al, 1964) Burnett et al, 1977; (Hall & Rumack, 1997).
    b) CASE REPORT: A 24-year-old man developed cardiac arrest after exposure to hydrogen sulfide. Following 2 hours of hyperbaric oxygen therapy and therapeutic hypothermia for 24 hours, his condition gradually improved. He was discharged after 5 days of hospitalization. After discharge, he experienced dysarthria, tunnel vision, numbness of his right arm, chronic headaches, and residual cognitive deficits, including poor working memory and a mild expressive aphasia (Asif & Exline, 2012).
    c) CASE REPORT: Bilaterally decreased activity in the putamen and the amygdala/hippocampal region, but no cortical perfusion abnormalities, was noted on a cerebral perfusion study (SPECT scan) 3.5 years following exposure to hydrogen sulfide gas (Schneider et al, 1998). Neuropsychological and neurofunctional testing revealed microsomia, psychomotor slowing, extrapyramidal signs, and memory deficits.
    d) CASE REPORT: Neurologic sequelae of profound motor dysfunction and mild cognitive dysfunction has been reported following hydrogen sulfide intoxication. A 25-year-old man was found unconscious after exposure to hydrogen sulfide. He presented with Glascow Coma Score of 5 and severe hypoxemia (pH 7.37, PaO2 46.7 mmHg, PaCO2 38.4 mmHg, HCO3 22 mmol/L). Neurologic examination revealed dysarthric speech, quadriparesis with increased muscle tone and Babinski response on both feet, memory loss, attention deficits and blunted affect. Brain magnetic resonance imaging (MRI) revealed abnormal signals in both basal ganglia and motor cortex (Nam et al, 2004).
    e) Inserra et al (2004) studied the neurobehavioral effects (cognitive, motor response, sensory, and mood/affect) of repeated and long-term exposure to moderate-to-low-level hydrogen sulfide. Chronic exposure was not associated with poorer performance on 26 of 28 neurobehavioral tests. Marginally poorer performance was observed in 2 tests (memory and the dynamometer grip strength tests); however, these differences were not statistically significant (Inserra et al, 2004).
    f) CASE REPORT: A 36-year-old man was found unconscious with no spontaneous respirations after exposure to hydrogen sulfide gas while cleaning a 50,000 gallon tank containing degrading eggs. He did not receive nitrite or hyperbaric oxygen therapies since he arrived to the hospital outside the therapeutic window of effectiveness and had good tissue oxygenation. A neurologic exam revealed spontaneous decerebrate posturing and up-going toes bilaterally. On day 2, a brain MRI with diffusion-weighted imaging revealed areas of restricted diffusion in the left superior cerebral hemisphere and in the left basal ganglia and thalamus, consistent with an anoxic brain injury. Following supportive care and intensive neuro-rehabilitation, he slowly improved over the next several months (Gerasimon et al, 2007).
    g) CASE REPORT: A 36-year-old man, with a history of epilepsy, presented unconscious with cyanosis, labored-breathing, bronchospasms, and generalized muscle twitching within 1 hour of exposure to hydrogen sulfide. He had 3 generalized tonic-clonic seizures within a 30-minute period. Despite supportive care, including treatment with nebulized salbutamol and ipratropium, benzodiazepines, a single dose of IV hydrocortisone, and antidote sodium nitrite (treated within 15 minutes of admission), he developed recurrent seizures, deepening unconsciousness, and decerebrate posturing. Following further treatment with parenteral barbiturates, phenytoin sodium, and sodium valproate, he regained consciousness and was extubated by day 3; however, he developed truncal ataxia and dysarthria while also complaining of recent, mild left-sided hearing impairment. He continued to use phenytoin monotherapy and his symptoms gradually improved over the next 2 weeks. On day 20, he was discharged with residual mild-dysarthria, mild ataxia, as well as retrograde amnesia of events (Shivanthan et al, 2013)
    D) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Generalized seizures are common with high exposures (Shivanthan et al, 2013; Christia-Lotter et al, 2007; Gunn & Wong, 2001; Tanaka et al, 1999; ATSDR, 1998; Hall & Rumack, 1997; Huang et al, 1997).
    E) SENSE OF SMELL ALTERED
    1) WITH POISONING/EXPOSURE
    a) Loss of sense of smell (anosmia) occurs at 50 ppm to 150 ppm and may take weeks to recover (Beauchamp, 1984).
    F) ABNORMAL NERVOUS SYSTEM FUNCTION
    1) WITH POISONING/EXPOSURE
    a) Persons with environmental exposure to hydrogen sulfide from "sour" crude oil processing facilities have been reported to have abnormal results on neuropsychological testing (Kilburn & Warshaw, 1995).
    b) Finnish residents in an area with several Kraft process pulp mills which release hydrogen sulfide and other sulfur compounds complained of headaches (Partti-Pellinen et al, 1996; Marttila et al, 1995; Marttila et al, 1994).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) HYPOXEMIA
    a) Wistar rats were exposed to hydrogen sulfide gas 800 mg/m(3) for 20 minutes. Analysis of neurons showed hypertrophy of the Golgi complex and decreases in the number of rough endoplasmic reticulum channels. All changes appeared to be reversible and showed a pattern similar to that seen in acute hypoxia.
    1) Rats exposed to the same dose per day for 3 days showed significant changes in the structure of myelin fibers with destruction of the of the axial cylinder, homogenization of the myelin sheath, delamination of plates of myelin into the axial cylinder, and the appearance of concentric layered myelin-like structures within varicose swellings of the axial cylinders (Solnyshkova et al, 2004).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Hydrogen sulfide irritates the mucous membranes producing nausea and vomiting (ATSDR, 1998; Audeau et al, 1985; Thoman, 1969).
    b) Finnish residents in an area with several Kraft process pulp mills which release hydrogen sulfide and other sulfur compounds complained of nausea (Partti-Pellinen et al, 1996; Marttila et al, 1995; Marttila et al, 1994).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ALBUMINURIA
    1) WITH POISONING/EXPOSURE
    a) Acute exposure may rarely cause albuminuria, cylindruria, and hematuria (ATSDR, 1998; Gosselin et al, 1984).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) LACTIC ACIDOSIS
    1) WITH POISONING/EXPOSURE
    a) Transient lactic acidosis may be noted following significant exposure, secondary to cellular hypoxia and seizures (Gerasimon et al, 2007; Nelson & Robinson, 2002; ATSDR, 1998; Tanaka et al, 1999).
    b) CASE REPORT: A 24-year-old oil well worker was found by emergency medical services unresponsive and in cardiac arrest after an explosion at work. He was taken to a local emergency department after resuscitation and intubation. At this time, a strong odor of rotten eggs, consistent with hydrogen sulfide exposure, was noted. Laboratory results revealed an acute uncompensated metabolic acidosis (pH 7.25, PCO2 40 mm Hg, PO2 332 mmHg, bicarbonate 14 mmol/L) and elevated troponin (0.27 ng/mL), suggesting myocardial ischemia. An ECG revealed sinus tachycardia. He was transported to an ICU after stabilization and decontamination. Following supportive care, laboratory results revealed improvement in the metabolic acidosis, pH of 7.43, bicarbonate of 22 mmol/L, lactate of 1.2 mmol/L, and troponin of 1.1 ng/mL. He was placed in a hyperbaric oxygen chamber 1 hour after arrival to the ICU (10 hours postexposure) and remained there for 2 hours. During therapy, he developed sinus bradycardia (HR, 40 to 60 beats/min) and hypotension, treated with a bolus of norepinephrine. Approximately 14 hours after the initial exposure, he underwent therapeutic hypothermia for 24 hours to treat his cardiac arrest. His condition improved gradually and he was discharged after 5 days of hospitalization. After discharge, he experienced dysarthria, tunnel vision, numbness of his right arm, chronic headaches, and residual cognitive deficits, including poor working memory and a mild expressive aphasia (Asif & Exline, 2012).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Skin exposure may result in severe pain, itching, burning, and erythema, especially in moist areas. Cyanosis may be noted.
    B) FROSTBITE
    1) WITH POISONING/EXPOSURE
    a) Direct contact with the liquefied material or escaping compressed gas can cause frostbite injury (AAR, 1996; (Sittig, 1991).

Reproductive

    3.20.1) SUMMARY
    A) Spontaneous abortions have occurred after exposure to life-threatening concentrations.
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY DISORDER
    1) Many reproductive studies of hydrogen sulfide exposed workers have been performed, but these generally involve mixed exposures with CARBON DISULFIDE, a known human reproductive hazard. Women employed in the viscose rayon industry have been extensively studied and have been found to be at increased risk for spontaneous abortions (Petrov, 1969; Vasilyeva, 1973) and longer menstrual cycles (Vasilyeva, 1973). Women exposed to a variety of chemicals including hydrogen sulfide were reported to have increased difficulties with pregnancy and labor (Sorokina, 1981). Exposure to carbon disulfide and other chemicals may be important confounders in these studies, as may be physical factors, such as lifting heavy weights.
    B) ABORTION
    1) Increased rates of spontaneous abortions were reported among women employed in rayon textile jobs and paper products jobs. However, there was only an insignificantly higher rate (9.3 vs 7.6) of spontaneous abortions noted in all socio-economic classes in areas where the mean annual level of hydrogen sulfide exceeded 4 micrograms/cubic meter (Hemminki & Niemi, 1982).
    2) Wives of men employed at a refinery who were predicted to be exposed to hydrogen sulfide were reported to be at twice the normal risk of having spontaneous abortions and stillbirths, but these risks were not linked specifically to hydrogen sulfide (Anon, 1982). An older review mentioned hydrogen sulfide in the context of causing damage to the testes and/or male reproduction (Hueper, 1942), but no confirmation of this association was found in more recent studies.
    3) An epidemiological study of 2853 Chinese female workers found an increased risk of spontaneous abortions associated with exposure to benzene, gasoline, and hydrogen sulfide (Xu et al, 1998).
    C) ANIMAL STUDIES
    1) In rats, fetal hydrogen sulfide exposure causes alterations of tissue monoamine levels in the developing brain (Roth et al, 1995).
    2) Hydrogen sulfide, when combined with carbon disulfide, was embryotoxic in the rat (Barilyak, 1975). Neurochemical changes are seen in rats exposed from gestational day 5 to post natal day 21 to low levels of hydrogen sulfide (Roth et al, 1995).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS7783-06-4 (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) In Rotorua, New Zealand (an active geothermal zone where hydrogen sulfide is released to the atmosphere), cancer deaths were not related to the extent of hydrogen sulfide exposure and there was no overall excess mortality found.
    3.21.3) HUMAN STUDIES
    A) LACK OF EFFECT
    1) In Rotorua, New Zealand (an active geothermal zone where hydrogen sulfide is released to the atmosphere), cancer deaths were not related to the extent of hydrogen sulfide exposure and there was no overall excess mortality found (Bates et al, 1998; Bates et al, 1997).

Genotoxicity

    A) Hydrogen sulfide exposure was associated with an increased risk of chromosome aberrations in chemical workers. Other factors may be involved in these multiply-exposed cohort populations.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Specific laboratory studies for confirming hydrogen sulfide exposure are not readily available in most clinical laboratories and are often not clinically useful.
    B) Monitor serum electrolytes, BUN, creatinine, glucose, CBC, CPK, urinalysis, and ECG.
    C) Monitor vital signs, pulse oximetry and/or arterial blood gases and chest radiograph in patients with respiratory signs or symptoms.
    D) In the acutely ill patient, blood gas analysis may demonstrate metabolic acidosis, and elevated mixed venous oxygen measurement. Lactate is also usually elevated.
    E) Hydrogen sulfide can also be measured in the environment by many emergency response teams using electrochemical sensors.
    F) Brain CT may reveal white matter demyelination and degeneration of the globus pallidus in patients with severe poisoning.
    G) Monitor methemoglobin levels if nitrite antidotes are administered.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Whole blood sulfide concentration in normal subjects is less than 0.05 mg/L (Baselt & Cravey, 1995).
    2) Reliable blood sulfide measurement requires that the sample be taken not later than two hours after the exposure and that it be analyzed immediately (Jappinen & Tenhunen, 1990). Such levels may be used to document the exposure, but are not useful for emergent diagnosis or to guide emergent treatment.
    3) ALA-S and Haem-S both decrease in activity, but the decrease is not correlated with the degree of exposure (Jappinen & Tenhunen, 1990; Tenhunen et al, 1983).
    4) In fatal cases, confirmation of hydrogen sulfide poisoning can be done by measuring both sulfide and thiosulfate levels in blood (Chaturvedi et al, 2001; Kage et al, 2002; Kage et al, 1997).
    5) Where hydrogen sulfide was present in the air, a blood sulfide concentration of 0.95 micromoles/L was measured in an adult female who was found dead beneath a pool of sewage in the pump room of a fish market that had detectable ambient hydrogen sulfide(Imamura et al, 1996).
    B) HEMATOLOGIC
    1) Sulfmethemoglobin levels transiently increase after nitrite treatment, but are difficult to measure (Reynolds, 1982).
    C) ACID/BASE
    1) Monitor pulse oximetry and/or arterial blood gases in patients with respiratory symptoms.
    4.1.3) URINE
    A) URINALYSIS
    1) Monitor urine output. Obtain urinalysis.
    2) Detection of thiosulfate in the urine is an indicator of hydrogen sulfide poisoning in nonfatal cases (Kage et al, 1997). However, interpretation of urinary thiosulfate levels may be confounded by dietary intake of food or water with high sulfur content (Torun et al, 1989).
    4.1.4) OTHER
    A) OTHER
    1) OTHER
    a) Detection of hydrogen sulfide odor (similar to rotten eggs) on the patient's clothing or breath may be indicative of exposure (Milby & Baselt, 1999).
    b) Silver coins in pockets of victims or rings on exposed fingers may turn black (Duong et al, 2001; Ellenhorn, 1997; Grant, 1993).
    c) Hydrogen sulfide in air can be detected with the use of lead acetate paper (ILO, 1983).

Methods

    A) ANALYTICAL METHODS
    1) A GC/MS method for qualification and quantitation of sulfide and thiosulfate in postmortem blood and tissue samples taken from a patient following exposure to hydrogen sulfide gas has been described (Kage et al, 1998). Analysis should be considered as soon as possible based on the rapid loss of sulfide from biological materials (Baselt & Cravey, 2000).
    2) Methods used to determine urinary thiosulfate levels have included colorimetry and gas and liquid chromatography. (Baselt & Cravey, 2000).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.3) DISPOSITION/INHALATION EXPOSURE
    6.3.3.1) ADMISSION CRITERIA/INHALATION
    A) Immediate supportive care should be given as most fatalities occur at the scene.
    1) The victim should be evacuated to fresh air.
    2) Maximum oxygen flow and supportive care may be sufficient treatment without the need to use nitrites (Ravizza et al, 1982). Seizures may have to be controlled with muscle relaxants (ie, succinylcholine) to complete intubation (Kemper, 1966).
    3) Keep victim quiet and maintain normal body temperature.
    4) Symptomatic patients have been kept under observation for an average of 48 hours (Burnett et al, 1977) and monitored closely for acute lung injury, dysrhythmias, peripheral neuritis, or some degree of neurological disturbance (Gosselin et al, 1984).
    6.3.3.2) HOME CRITERIA/INHALATION
    A) All significant exposures should be sent to a hospital.
    6.3.3.3) CONSULT CRITERIA/INHALATION
    A) Consult a medical toxicologist or a poison center for any severely poisoned patient. Data are controversial regarding hyperbaric therapy; however, if a hyperbaric center is readily available, contact a hyperbaric specialist to consult on a patient with severe poisoning. Consult an ophthalmologist for patients with keratoconjunctivitis or corneal ulceration.
    6.3.3.5) OBSERVATION CRITERIA/INHALATION
    A) Patients who are minimally symptomatic may be observed until resolution of symptoms in a healthcare facility.

Monitoring

    A) Specific laboratory studies for confirming hydrogen sulfide exposure are not readily available in most clinical laboratories and are often not clinically useful.
    B) Monitor serum electrolytes, BUN, creatinine, glucose, CBC, CPK, urinalysis, and ECG.
    C) Monitor vital signs, pulse oximetry and/or arterial blood gases and chest radiograph in patients with respiratory signs or symptoms.
    D) In the acutely ill patient, blood gas analysis may demonstrate metabolic acidosis, and elevated mixed venous oxygen measurement. Lactate is also usually elevated.
    E) Hydrogen sulfide can also be measured in the environment by many emergency response teams using electrochemical sensors.
    F) Brain CT may reveal white matter demyelination and degeneration of the globus pallidus in patients with severe poisoning.
    G) Monitor methemoglobin levels if nitrite antidotes are administered.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Hydrogen sulfide is a gas at room temperature, making ingestion unlikely.
    2) Move the victim to an area of fresh air and immediately provide respiratory support using 100% humidified oxygen.
    3) Although its efficacy is still unproven, nitrite therapy is recommended if it can be started early.
    4) Hyperbaric oxygen may be given to those who continue to be symptomatic after standard therapy.
    5) Measures should be taken to control seizures, pulmonary edema, and dysrhythmias and to correct hypotension.
    6) Exposed mucocutaneous surfaces should be thoroughly washed with copious amounts of soap and water.
    7) Rescuers should wear a self-contained breathing apparatus, special chemical protective clothing, and a safety line during rescue operations. Many would-be rescuers have become victims when entering contaminated enclosed areas without proper protective equipment.
    8) Observe for delayed onset (up to 72 hours) of acute respiratory effects.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Hydrogen sulfide is a gas at room temperature (Harbison, 1998), making ingestion unlikely.
    6.5.3) TREATMENT
    A) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Immediately move the patient to fresh air and administer 100% oxygen. Prevent self-exposure and possible death by wearing a self-contained breathing apparatus to rescue the victim.
    B) Prompt termination of exposure to even extremely high vapor concentrations (eg, 1000 ppm) may result in rapid recovery (Gosselin et al, 1984).
    C) Keep patient warm and at rest.
    6.7.2) TREATMENT
    A) OXYGEN
    1) Administer 100% oxygen. It may diminish the toxic effects of hydrogen sulfide (Beck et al, 1981; Ravizza et al, 1982).
    B) 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).
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) DRUG THERAPY
    1) SODIUM NITRITE
    a) Sodium nitrite MAY be beneficial in preventing severe anoxia by converting hemoglobin to methemoglobin and protecting the cytochrome oxidase enzyme (Peters, 1981). Do NOT administer sodium thiosulfate.
    1) INDICATION
    a) Sodium nitrite should be given initially and administered as soon as vascular access is established.
    b) Further administration of sodium nitrite is dictated only by the clinical situation, provided no significant complications (hypotension, excessive methemoglobinemia) are present. Use with caution if carbon monoxide poisoning is also suspected.
    c) The goal of nitrite therapy is to achieve a methemoglobin level of 20% to 30%. This level is not based on clinical data, but represents the tolerated concentration without significant adverse symptoms from methemoglobin in an otherwise healthy individual. Clinical response has been reported to occur with methemoglobin levels in the range of 3.6% to 9.2% (DiNapoli et al, 1989; Johnson et al, 1989; Johnson & Mellors, 1988).
    2) ADULT DOSE
    a) 10 mL of a 3% solution (300 mg) administered intravenously at a rate of 2.5 to 5 mL/minute (Prod Info NITHIODOTE intravenous injection solution, 2011). Frequent blood pressure monitoring must accompany sodium nitrite injection and the rate slowed if hypotension occurs.
    b) If there is inadequate clinical response, an additional dose of sodium nitrite at half the amount of the initial dose may be administered 30 minutes following the first dose (Prod Info NITHIODOTE intravenous injection solution, 2011).
    3) PEDIATRIC DOSE
    a) The recommended pediatric sodium nitrite dose is 0.2 mL/kg of a 3% solution (6 mg/kg) administered intravenously at a rate of 2.5 to 5 mL/minute, not to exceed 10 mL (300 mg) (Prod Info NITHIODOTE intravenous injection solution, 2011).
    b) If there is inadequate clinical response, an additional dose of sodium nitrite at half the amount of the initial dose may be administered 30 minutes following the first dose (Prod Info NITHIODOTE intravenous injection solution, 2011; Berlin, 1970).
    c) PRESENCE OF ANEMIA: If there is a reason to suspect the presence of anemia, the following initial sodium nitrite doses should be given, depending on the child's hemoglobin (sodium nitrite should not exceed the doses listed below; fatal methemoglobinemia may result) (Berlin, 1970):
    1) Hemoglobin: 8 g/dL - Initial 3% sodium nitrite dose: 0.22 mL/kg (6.6 mg/kg)
    2) Hemoglobin: 10 g/dL - Initial 3% sodium nitrite dose: 0.27 mL/kg (8.7 mg/kg)
    3) Hemoglobin: 12 g/dL (average child) - Initial 3% sodium nitrite dose: 0.33 mL/kg (10 mg/kg)
    4) Hemoglobin: 14 g/dL - Initial 3% sodium nitrite dose: 0.39 mL/kg (11.6 mg/kg)
    b) The antidotal action of sodium nitrite is attributed to a competition for free sulfide between tissue cytochrome oxidase and circulating methemoglobin, the latter binding sulfide in an inactive form called sulfmethemoglobin which in turn slowly releases sulfide to endogenous detoxification processes (Scheler & Kabisch, 1963; Smith & Gosselin, 1964). The freed cytochrome oxidase then reactivates aerobic metabolism.
    c) The antidotal efficacy of nitrite therapy is controversial.
    d) The injection of sodium nitrite has been employed successfully in the resuscitation of 2 human victims of severe hydrogen sulfide poisoning (Peters, 1981; Stine et al, 1976) and appeared to have some clinical efficacy in 2 other cases (Hall & Rumack, 1997).
    e) In an in vitro study demonstrated that sulfide is rapidly oxidized (90% in 20 minutes) to sulfur and sulfur oxides by oxyhemoglobin. Because ventilation also produces conditions which actually slow sulfide removal, nitrite as an antidote was expected to be effective only within the first few minutes after exposure (Beck et al, 1981).
    1) These authors contend that the length of time it takes to induce methemoglobinemia make the nitrite protocol too slow, inappropriate, and potentially hazardous, and that oxygen therapy is the only effective treatment for hydrogen sulfide intoxication. However, until further studies are available, nitrite therapy is recommended if it can be started early in patients with severe effects, generally within 1 hour of exposure.
    f) ADVERSE EFFECTS: Sodium nitrite may rarely produce elevated methemoglobin concentrations even when standard doses are administered. Hypotension from vasodilation may be avoided if sodium nitrite is given IV push. Administer over 5 minutes in the undiluted form, or by diluting the drug in 50 to 100 mL D5W followed by infusion with frequent monitoring using the fastest rate that does not decrease the blood pressure (Hall & Rumack, 1997).
    E) ACUTE LUNG INJURY
    1) Patients should be monitored closely for the development of acute lung injury; positive end expiratory pressure may be useful.
    2) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    3) 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)
    4) 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).
    5) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    6) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    7) 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).
    8) 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).
    F) MONITORING OF PATIENT
    1) Specific laboratory studies for confirming hydrogen sulfide exposure are not readily available in most clinical laboratories and are often not clinically useful.
    2) Monitor serum electrolytes, BUN, creatinine, glucose, CBC, CPK, urinalysis, and ECG.
    3) Monitor vital signs, pulse oximetry and/or arterial blood gases and chest radiograph in patients with respiratory signs or symptoms.
    4) In the acutely ill patient, blood gas analysis may demonstrate metabolic acidosis, and elevated mixed venous oxygen measurement. Lactate is also usually elevated.
    5) Hydrogen sulfide can also be measured in the environment by many emergency response teams using electrochemical sensors.
    6) Brain CT may reveal white matter demyelination and degeneration of the globus pallidus in patients with severe poisoning.
    7) Monitor methemoglobin levels if nitrite antidotes are administered.
    G) HYPERBARIC OXYGEN THERAPY
    1) Several anecdotal case studies suggest that hyperbaric oxygen may be useful for severe hydrogen sulfide toxicity (Gunn & Wong, 2001). Although patients who continue to have significant toxicity after standard therapy may benefit from hyperbaric oxygen, the clinical efficacy of this modality remains to be determined.
    a) Hyperbaric oxygen therapy (HBO) can reduce cerebral edema and promote the elimination of hydrogen sulfide from the mitochondrial cytochrome oxidase. In one study, 21 patients with acute occupational hydrogen sulfide intoxication presented during a 1-year period and received HBO (using a carbon monoxide protocol) by either a mask (n=15; mild intoxications) or by an endo-tracheal tube (n=6; severe intoxications). Patients with severe toxicity also received 4-DMAP 3 mg/kg IV immediately preceding the HBO therapy. The carbon monoxide protocol consisted of 3 HBO treatments within the first 24-hour (3 atmospheres absolute [ATA] for 60 min, 2.2 ATA for 30 min), followed by a single HBO treatment (2.2 ATA for 90 min) every following day. In addition, patients received mucolytics, bronchodilators, corticosteroids, and antibiotics, while oxygen supply was continued. In the severe group, CT scan revealed cerebral edema and ischemia in 3 patients and toxic lung edema in 2 patients. After clinical symptoms resolved and methemoglobin concentrations normalized, HBO therapy was discontinued. All patients received an average of 3.8 HBO therapies. Death from irreversible cerebral and pulmonary edema occurred in 2 patients. The rest of the patients (n=19) recovered and were discharged after a median of 2.8 days. All patients in the mild group were discharged the next day (Lindenmann et al, 2010).
    b) Two severely symptomatic patients with hydrogen sulfide poisoning were noted to have marked improvement following hyperbaric oxygen therapy after failing to improve with 100% oxygen and nitrites (Smilkstein et al, 1985; Whitcraft et al, 1985). HBO was effective in the first case, even though initiated 10 hours postexposure and in another case, also started 10 hours postexposure (Schneider et al, 1998).
    c) CASE REPORT: A 24-year-old oil well worker was found by emergency medical services unresponsive and in cardiac arrest after an explosion at work. He was taken to a local emergency department after resuscitation and intubation. At this time, a strong odor of rotten eggs, consistent with hydrogen sulfide exposure, was noted. Laboratory results revealed an acute uncompensated metabolic acidosis (pH 7.25, PCO2 40 mm Hg, PO2 332 mmHg, bicarbonate 14 mmol/L) and elevated troponin (0.27 ng/mL), suggesting myocardial ischemia. An ECG revealed sinus tachycardia. He was transported to an ICU after stabilization and decontamination. Following supportive care, laboratory results revealed improvement in the metabolic acidosis, pH of 7.43, bicarbonate of 22 mmol/L, lactate of 1.2 mmol/L, and troponin of 1.1 ng/mL. He was placed in a hyperbaric oxygen chamber 1 hour after arrival to the ICU (10 hours postexposure) and remained there for 2 hours. During therapy, he developed sinus bradycardia (HR, 40 to 60 beats/min) and hypotension, treated with a bolus of norepinephrine. Approximately 14 hours after the initial exposure, he underwent therapeutic hypothermia for 24 hours to treat his cardiac arrest. His condition improved gradually and he was discharged after 5 days of hospitalization. After discharge, he experienced dysarthria, tunnel vision, numbness of his right arm, chronic headaches, and residual cognitive deficits, including poor working memory and a mild expressive aphasia (Asif & Exline, 2012).
    d) CASE REPORT: A 30-year-old man exposed to hydrogen sulfide through working with hydrogen sulfide-contaminated petroleum underwent 3 hyperbaric oxygen treatments 13 hours postexposure. Improvement in memory, verbal interactions, problem solving, and left-sided weakness was observed, though retrograde amnesia continued (Vicas et al, 1989).
    e) CASE REPORT: A patient received hyperbaric oxygen therapy after an acute exposure to a high concentration of hydrogen sulfide gas and after initial treatment with sodium nitrite and 100% oxygen failed to improved his arterial blood gases (ie, pH). No improvement was seen after 3 hours of hyperbaric oxygen therapy, and the patient died 56 hours after exposure. At autopsy, blood sulfide levels were normal, suggesting that early administration of hyperbaric oxygen therapy might be of greater therapeutic value (Al-Mahasneh et al, 1989).
    2) In an acute experimental sulfide poisoning study in the rat, the best therapeutic regimen tested was a combination of 3 ATA oxygen and sodium nitrite administration following intraperitoneal injection of an LD75 dose of sulfide (Bitterman et al, 1986). Additional studies are needed before this treatment can be routinely recommended in humans.
    H) EXPERIMENTAL THERAPY
    1) HYDROXOCOBALAMIN
    a) CASE REPORT: A man was found unconscious and not breathing after exposure to hydrogen sulfide gas produced by mixing 2 commercial products in a suicide attempt. On presentation, an ECG revealed asystole. Laboratory results revealed an arterial carboxyhemoglobin of 1.5%, indicating no carbon monoxide poisoning. He died 42 minutes after presentation, despite supportive care, including cardiopulmonary resuscitation and treatment with hydroxocobalamin 2.5 g IV infusion. Serum concentrations of sulfide and thiosulfide before hydroxocobalamin therapy were 0.22 mcg/mL and 0.34 micromol/mL, respectively. Following hydroxocobalamin therapy, serum concentrations of sulfide and thiosulfide decreased to 0.11 mcg/mL and 0.04 micromol/mL, respectively. It is determined that hydroxocobalamin will form a complex with hydrogen sulfide which in turn metabolizes to thiosulfate and sulfate and then excreted. Since thiosulfate concentration was decreased, it is suggested that hydroxocobalamin and thiosulfate also form a complex. In addition, hydroxocobalamin has a higher affinity for thiosulfate than for hydrogen sulfide, as the concentration of thiosulfate decreased to a greater extent than did sulfide. Although in this case, hydroxocobalamin was not effective, the decrease in serum concentration of hydrogen sulfide's metabolites suggests that this therapy may be effective if used immediately after hydrogen sulfide exposure. However, more studies are warranted (Fujita et al, 2011).
    2) CORBINAMIDE
    a) In one animal study using a swine model, none of the animals in the control group survived longer than 5 minutes after apnea was produced following hydrogen sulfide exposure; however, all corbinamide-treated animals survived for the entire 60-minute observation period (Bebarta et al, 2015).
    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) SUPPORT
    1) Treatment of keratoconjunctivitis is symptomatic and supportive. The goal of therapy is to provide an opportunity for spontaneous healing of the epithelium. Local anesthetics should only be used at the initial examination. A brief-acting mydriatic-cycloplegic, a bland antibiotic ointment, bedrest with the eyes closed, and a systemic analgesic such as aspirin for the discomfort has been suggested (Grant, 1993).
    B) SUPPORT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    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) FROSTBITE
    1) PREHOSPITAL
    a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).
    2) REWARMING
    a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
    b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
    c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
    d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).
    3) WOUND CARE
    a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
    b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
    c) The injured extremities should be elevated and should not be allowed to bear weight.
    d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
    e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
    f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
    g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
    h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
    i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
    j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
    k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
    l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
    m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
    n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).
    B) GENERAL TREATMENT
    1) Treatment should include recommendations listed in the INHALATION EXPOSURE section when appropriate.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Abstracts

Case Reports

    A) ADULT
    1) Following a massive inhalation of hydrogen sulfide, a 22-year-old man presented with a Glasgow coma scale score of 7, prolonged seizures, and severe dyspnea. In the ICU, he had bilateral myosis, tachycardia, hypotension, and hyperthermia at 38 degrees Celsius. Laboratory results showed elevated total CPK and normal troponin level. ECG and ultrasound revealed severe posterolateral hypokinesis of the cardiac muscle. Less than 24 hours after admission to ICU, he died with acute respiratory distress complicated by severe hemodynamic insufficiency due to myocardial necrosis. Autopsy showed cerebral edema and anoxic brain injury, myocardial necrosis, and aspiration pneumonia (Christia-Lotter et al, 2007).
    2) A 36-year-old man was found unconscious with no spontaneous respirations after exposure to hydrogen sulfide gas while cleaning a 50,000 gallon tank containing degrading eggs. In the ICU, approximately 45 to 60 minutes following exposure, he had fever, hypertension, sinus tachycardia (141 BPM), and mild lactic acidosis which normalized over the next day. A chest radiograph showed mild pulmonary edema; however, he did not experience any late or long-term sequelae from his acute lung injury. He did not receive nitrite or hyperbaric oxygen therapies since he arrived to the hospital outside the therapeutic window of effectiveness and had good tissue oxygenation. A neurologic exam revealed spontaneous decerebrate posturing and upgoing toes bilaterally. On day 2, a brain MRI with diffusion-weighted imaging revealed areas of restricted diffusion in the left superior cerebral hemisphere and in the left basal ganglia and thalamus, consistent with an anoxic brain injury. Following supportive care and intensive neuro-rehabilitation, he slowly improved over the next several months (Gerasimon et al, 2007).
    3) A 30-year-old male, found unconscious after loading a truck with hydrogen sulfide-contaminated petroleum, was given general supportive care and administration of oxygen. Minimal improvement in mental status was observed. At thirteen hours postexposure, three hyperbaric oxygen treatments were instituted, which resulted in improvements in verbal interactions, memory, problem solving, and left-sided weakness. Retrograde amnesia continued to be observed (Vicas et al, 1989).
    4) A 45-year-old man was exposed to high concentrations of hydrogen sulfide gas while cleaning a hospital cast room drain with 90% sulfuric acid (Peters, 1981). He was noted to be apneic, comatose and cyanotic after being moved to an outdoor area 2 to 3 minutes following the exposure.
    a) Methemoglobinemia was induced within 30 minutes after the incident with inhalation of amyl nitrite and intravenous injection of sodium nitrite. A normal mental status was noted approximately 6 hours after the exposure. The sulfhemoglobin level was 7.9% (normal, less than 0.5%).
    5) A 35-year-old man who worked in a chemical manufacturing factory died secondary to hydrogen sulfide (H2S) poisoning. The factory's ambient H2S concentration was unknown, but blood gas analysis of the victim showed a sulfide concentration of 1.1 ppm (reference level 0.03 ppm). On autopsy, green discoloration of the victim's brain tissue was found; the discoloration was concentrated in the grey matter and nuclei. No other remarkable pathological changes were noted (Park et al, 2009).

Range Of Toxicity

Summary

    A) Concentrations of 50 to 100 ppm are associated with mild toxicity manifesting as respiratory tract irritation while concentrations greater than 500 ppm are usually associated with the loss of consciousness and death.
    B) At an airborne concentration of 0.05 ppm, hydrogen sulfide produces a characteristic odor of rotten eggs. The distinctive rotten egg odor cannot be detected at concentrations above 150 ppm.
    C) Exposure to greater than 500 ppm results in severe toxicity and death. Respiratory paralysis and death may be noted within 30 to 60 minutes. At 800 to 1000 ppm, death may be nearly immediate after 1 or more breaths.

Minimum Lethal Exposure

    A) ROUTE OF EXPOSURE
    1) Concentrations of 0.1 to 0.2% in the atmosphere may be fatal in a few minutes. Toxicity to the CNS could occur suddenly with concentrations in excess of 500 ppm and immediate death might follow concentrations in excess of 1000 ppm (OHM/TADS , 1999; Lewis, 1996).
    2) Coma and death from respiratory arrest occur with exposure to concentrations between 500 and 1000 ppm (ACGIH, 1986). A single breath at concentrations of 1000 ppm or greater may cause coma and respiratory arrest (Hathaway et al, 1996).
    3) CASE REPORT: After entering an empty tank of a fish hatchery, an adult lost consciousness and did not recover. Prior to emptying the fish tank, the hydrogen sulfide levels in the water was 4 mg/L (Nikkanen & Burns, 2004).
    4) CASE REPORT: Four fatalities in two separate accidents involving wastewater industrial workers have been reported. In the first accident, three men were working next to a receiving silo in an unconfined room at the same time a truck was dumping several tons of sludge from wastewater purification stations. The first man was checking a pump mechanism close to the silo when be suddenly became unconscious. The two fellow coworkers went to his aid and quickly lost consciousness. All three workers died at the scene. Autopsy reports revealed sulfide levels from all three victims as 2.48, 14.9 and 18.1 mg/L, respectively. Environmental teams detected levels of 100 ppm of hydrogen sulfide 6 hours after the accident. In the second accident, one man lost consciousness while descending a staircase shortly after a pulse of hydrogen sulfide gas was released into an unconfined space from an evacuation window located close to the staircase. He received medical care within 15 minutes of exposure; however, he did not survive(Nogue et al, 2011).

Maximum Tolerated Exposure

    A) CONCENTRATION LEVEL
    1) Olfactory fatigue occurs at concentrations of 100 ppm and at concentrations of 150 ppm, the odor of hydrogen sulfide disappears secondary to olfactory paralysis, making perception of odor an unreliable warning property (Caravati, 2004; Hendrickson et al, 2004).
    2) Exposure to airborne concentrations greater than 50 ppm results in gradually worsening signs and symptoms, and with exposure to greater than 500 ppm there is immediate loss of consciousness, depressed respirations, and death in 30 to 60 minutes (OHM/TADS , 1999; Lewis, 1996; ACGIH, 1992; Hathaway et al, 1996).
    Hydrogen Sulfate Concentrations and Expected Effects (ACGIH, 1992; Hathaway et al, 1996; Guidotti, 1996)
    EFFECTSH2S CONCENTRATIONONSET
    Eye Irritation4 to 100 ppm 
    Respiratory Irritation; (possible pulmonary edema)50 to 500 ppm 
    Bronchitis and/or acute lung injury250 ppm24 to 72 hours
    Symptomatic50 ppm for0.5 hour
    Severely toxic200 ppm for1 minute
    Coma and death500 to 1000 ppm 
    Fatal800 ppmimmediate
    600 ppm30 minutes
    Breathing ceases with 1 to 2 breaths (immediate collapse)1000 ppmimmediate

    3) Another source reported the hydrogen sulfide and expected effects: 0.15 ppm, detectable odor; 150 ppm, olfactory nerve paralysis, mucous membrane irritation; 500 ppm, headache, pulmonary edema; 700 ppm, loss of consciousness; 1000 ppm, convulsions, coma, respiratory paralysis, death. It has been suggested that paralysis of the olfactory nerve may occur. The loss of perception of the odor as the levels increases has been described as "olfactory extinction" (Nikkanen & Burns, 2004).
    4) Because the human body has an inherently large capacity for detoxifying sulfide (Haggard, 1925; Weber & Lendle, 1965), the toxicity is more closely related to concentration than to length of exposure (O'Donoghue, 1961; Smith & Gosselin, 1964).
    5) Men and women can safely perform work of moderate intensity in environments with 5 ppm of airborne hydrogen sulfide (Bhambhani et al, 1994; Bhambhani et al, 1996).
    a) At an airborne hydrogen sulfide concentration of 10 ppm, there was a decrease in oxygen uptake and an increase in serum lactic acid levels during exercise but no changes in arterial blood values or cardiovascular parameter alterations were found (Bhambhani et al, 1997).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) SPECIFIC SUBSTANCE
    a) Sulfide ion levels measured soon after death from hydrogen sulfide poisoning ranged from 0.9 to 3.75 mg/L (Winek et al, 1968; McAnalley et al, 1979). Postmortem confirmation of toxic levels is complicated by rapid endogenous destruction of sulfide ion and formation of sulfide from postmortem protein degradation (Evans, 1967).
    b) Tissue sulfide concentrations in a workman fatally exposed in a tank containing up to 6100 ppm of hydrogen sulfide gas were as follows (Baselt & Cravey, 1995) -
    1) Blood - 0.92 mg/L
    2) Brain - 1.06 mg/kg
    3) Liver - 0.38 mg/kg
    4) Kidney - 0.34 mg/kg
    c) Tissue sulfide and thiosulfate concentrations in a geothermal power plant worker fatally exposed to an estimated 3500 to 5000 ppm of hydrogen sulfide gas were as follows (Kage et al, 1998):
    .SULFIDETHIOSULFATE
    Blood0.45 mcg/mL (0.014 mmol/mL)16.02 mcg/mL (0.143 mmol/mL)
    Brain2.72 mcg/mL (0.085 mmol/mL)5.04 mcg/mL (0.045 mmol/mL)
    Lung0.42 mcg/mL (0.013 mmol/mL)9.30 mcg/mL (0.083 mmol/mL)
    Fem muscle0.16 mcg/mL (0.005 mmol/mL) .

    d) Post mortem blood sulfide level in one case was 1.68 mcg/mL (Chaturvedi et al, 2001).
    e) In another case report, thiosulfate concentration in whole blood was 10.53 and 4.59 mg/L postmortem in two fatalities compared with plasma thiosulfate concentration of 4.14 mg/L and below 0.3 mg/L in two surviving patients (2 and 6 hours after exposure respectively) (Kage et al, 2002).
    f) Fatal hydrogen sulfide poisoning occurred by inhalation in 4 workers at a dye works in Japan. At autopsy, whole blood sulfide levels ranged from 0.32 to 9.36 mg/L and thiosulfate levels ranged from 0.11 to 0.23 mmol/L. Thiosulfate was not detected in the urine of the workers which indicated that all 4 men died within 1 hour after exposure (Kage et al, 2004).

Workplace Standards

    A) ACGIH TLV Values for CAS7783-06-4 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
    a) Adopted Value
    1) Hydrogen sulfide
    a) TLV:
    1) TLV-TWA: 1 ppm
    2) TLV-STEL: 5 ppm
    3) TLV-Ceiling:
    b) Notations and Endnotes:
    1) Carcinogenicity Category: Not Listed
    2) Codes: Not Listed
    3) Definitions: Not Listed
    c) TLV Basis - Critical Effect(s): URT irr; CNS impair
    d) Molecular Weight: 34.08
    1) For gases and vapors, to convert the TLV from ppm to mg/m(3):
    a) [(TLV in ppm)(gram molecular weight of substance)]/24.45
    2) For gases and vapors, to convert the TLV from mg/m(3) to ppm:
    a) [(TLV in mg/m(3))(24.45)]/gram molecular weight of substance
    e) Additional information:

    B) NIOSH REL and IDLH Values for CAS7783-06-4 (National Institute for Occupational Safety and Health, 2007):
    1) Listed as: Hydrogen sulfide
    2) REL:
    a) TWA:
    b) STEL:
    c) Ceiling: 10 ppm (15 mg/m(3)) [10-minute]
    d) Carcinogen Listing: (Not Listed) Not Listed
    e) Skin Designation: Not Listed
    f) Note(s):
    3) IDLH:
    a) IDLH: 100 ppm
    b) Note(s): Not Listed

    C) Carcinogenicity Ratings for CAS7783-06-4 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Hydrogen sulfide
    2) EPA (U.S. Environmental Protection Agency, 2011): Not applicable. This substance was not assessed using the EPA's 1986 cancer guidelines. ; Listed as: Hydrogen sulfide
    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 ; Listed as: Hydrogen sulfide
    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 CAS7783-06-4 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Listed as: Hydrogen sulfide
    2) Table Z-1 for Hydrogen sulfide:
    a) 8-hour TWA:
    1) ppm:
    a) Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.
    2) mg/m3:
    a) Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.
    3) Ceiling Value:
    4) Skin Designation: No
    5) Notation(s): Not Listed
    3) Table Z-2 for Hydrogen sulfide (Z37.2-1966):
    a) 8-hour TWA:
    b) Acceptable Ceiling Concentration: 20 ppm
    c) Acceptable Maximum Peak above the Ceiling Concentration for an 8-hour Shift:
    1) Concentration: 50 ppm
    2) Maximum Duration: 10 min. once, only if no other meas. exp. Occurs
    d) Notation(s): Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: RTECS, 2002

Pharmacology Toxicology

Toxicologic Mechanism

    A) Hydrogen sulfide inhibits cytochrome oxidase enzymes by binding to the iron in cytochrome oxidase a3. This disrupts the electron transport chain and aerobic metabolism, leading to anoxic and direct damage to the cells of the CNS. Anaerobic metabolism further causes lactic acidosis (Harbison, 1998).
    B) In experimental animals, hydrogen sulfide exposure inhibited neuronal cytochrome C oxidase and carbonic anhydrase in the brain, depolarized intraterminal mitochondria, and decreased oxygen consumption and adenosine triphosphate levels (Nicholson et al, 1998). Inhibition of CNS cellular respiratory enzymes may be the mechanism for hydrogen sulfide-induced alterations in brain structures such as the hippocampus (Roth et al, 1997).
    C) Rapid transitory effects such as dizziness, incoordination, abrupt physical collapse or "knock down", and headache are likely due to a direct toxic effect of hydrogen sulfide on the brain, while other effects are probably a consequence of hypoxia (Milby & Baselt, 1999).

Physicochemical

Physical Characteristics

    A) Hydrogen sulfide is a colorless gas with a rotten-egg odor perceptible in air at a concentration of 0.02 to 0.13 ppm (Budavari, 1996)
    B) Hydrogen sulfide is a flammable, heavier-than-air, colorless gas with a strong, offensive sulfur or "rotten eggs" odor and a sweetish taste (AAR, 1996; NIOSH, 1999; NFPA, 1986; (Lewis, 1996; Lewis, 1993; Budavari, 1996; CHRIS , 1999).
    1) Olfactory fatigue rapidly develops in hydrogen sulfide contaminated atmospheres, and perception of the odor is not reliable to warn of the continued presence of this gas (AAR, 1996).
    C) Hydrogen sulfide sinks in and boils in water, producing a poisonous, visible, flammable vapor cloud (CHRIS , 1999).
    D) Hydrogen sulfide burns with a pale blue flame in air (Budavari, 1996).

Ph

    A) The pH of a freshly prepared solution of water, glycerol, and hydrogen sulfide is 4.5 (Budavari, 1996).

Molecular Weight

    A) 34.08 (RTECS , 1999)

Other

    A) ODOR THRESHOLD
    1) 0.0047 ppm (CHRIS , 2002)

References

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