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Hydrogen sulfide is a highly toxic, flammable, colorless gas that is heavier than air. It is produced naturally by decaying organic matter and is also a by-product of many industrial processes. Hazardous levels may be found in petroleum refineries, tanneries, mines, pulp-making factories, sulfur hot springs, carbon disulfide production, commercial fishing holds, hot asphalt fumes, and pools of sewage sludge or liquid manure. It sometimes is referred to as “pit gas.” There have been reports of suicide by mixing acid-containing household cleaners with calcium sulfide–containing bath salts to generate hydrogen sulfide gas.

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  1. Mechanism of toxicity. Hydrogen sulfide causes cellular asphyxia by inhibition of the cytochrome oxidase system, similar to the action of cyanide. Because it is absorbed rapidly by inhalation, symptoms occur nearly immediately after exposure, leading to rapid unconsciousness, or “knockdown.” Hydrogen sulfide is also a mucous membrane irritant.

  2. Toxic dose. The characteristic rotten egg odor of hydrogen sulfide is detectable at concentrations as low as 0.025 ppm. The recommended workplace limit (ACGIH TLV-TWA) is 10 ppm (14 mg/m3) as an 8-hour time-weighted average, with a short-term exposure limit (STEL) of 15 ppm (21 mg/m3). The federal OSHA permissible exposure limit (PEL) is 20 ppm as a 15-minute ceiling during an 8-hour workday. Marked respiratory tract irritation occurs with levels of 50–100 ppm. Olfactory nerve paralysis occurs with levels of 100–150 ppm. The level considered immediately dangerous to life or health (IDLH) is 100 ppm. Pulmonary edema occurs at levels of 300–500 ppm. Levels of 600–800 ppm are rapidly fatal.

  3. Clinical presentation

    1. Irritant effects. Upper airway irritation, burning eyes, and blepharospasm may occur at relatively low levels. Skin exposure can cause painful dermatitis. Chemical pneumonitis and noncardiogenic pulmonary edema may occur after a delay of several hours.

    2. Acute systemic effects include headache, nausea and vomiting, dizziness, confusion, seizures, and coma. Massive exposure may cause immediate cardiovascular collapse, respiratory arrest, and death. Survivors may be left with serious neurologic impairment.

  4. Diagnosis is based on a history of exposure and rapidly progressive manifestations of airway irritation and cellular asphyxia, with sudden collapse. The victim or co-workers may describe the smell of rotten eggs, but because of olfactory nerve paralysis, the absence of this odor does not rule out exposure. Silver coins in the pockets of victims have been blackened (by conversion to silver sulfide). Greenish discoloration of the brain has been reported at autopsy.

    1. Specific levels are not generally available (sulfide is unstable in vitro), although elevated whole-blood sulfide and thiosulfate have been measured post mortem. Sulfhemoglobin is not thought to be produced after hydrogen sulfide exposure.

    2. Other useful laboratory studies include electrolytes, glucose, arterial blood gases, and chest radiography.

  5. Treatment

    1. Emergency and supportive measures. Note: Rescuers should use self-contained breathing apparatus to prevent personal exposure.

      1. Maintain an open airway and assist ventilation if necessary (See Airway and Breathing). Administer high-flow humidified supplemental oxygen. Observe for several hours for delayed-onset chemical pneumonia or pulmonary edema (See Hypoxia).

      2. Treat coma ...

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