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Sulfur dioxide is a colorless, nonflammable gas formed by the burning of materials that contain sulfur. It is a major air pollutant from automobiles, smelters, and plants that burn soft coal or oils with a high sulfur content. It is soluble in water to form sulfurous acid, which may be oxidized to sulfuric acid; both are components of acid rain. Occupational exposures to sulfur dioxide occur in ore and metal refining, chemical manufacturing, and wood pulp treatment and in its use as a disinfectant, refrigerant, and dried-food preservative.

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  1. Mechanism of toxicity. Sulfur dioxide is an irritant because it rapidly forms sulfurous acid on contact with moist mucous membranes. Most effects occur in the upper respiratory tract because 90% of inhaled sulfur dioxide is deposited rapidly there, but with very large exposures, sufficient gas reaches the lower airways to cause chemical pneumonitis and pulmonary edema.

  2. Toxic dose. The sharp odor or taste of sulfur dioxide is noticed at 1–5 ppm. Throat and conjunctival irritation begins at 8–12 ppm and is severe at 50 ppm. The ACGIH-recommended workplace permissible limit (TLV) is 0.25 ppm (0.65 mg/m3) as a short-term exposure limit (STEL). The NIOSH-recommended 8-hour time-weighted average is 2 ppm, and its recommended STEL is 5 ppm (13 mg/m3); the air level considered immediately dangerous to life or health (IDLH) is 100 ppm. Persons with asthma may experience bronchospasm with brief exposure to 0.5–1 ppm.

  3. Clinical presentation

    1. Acute exposure causes burning of the eyes, nose, and throat; lacrimation; and cough. Laryngospasm may occur. Wheezing may be seen in normal subjects as well as persons with asthma. Chemical bronchitis is not uncommon. With a very high-level exposure, chemical pneumonitis and noncardiogenic pulmonary edema may occur.

    2. Asthma and chronic bronchitis may be exacerbated.

    3. Sulfhemoglobinemia resulting from absorption of sulfur has been reported.

    4. Frostbite injury to the skin may occur from exposure to liquid sulfur dioxide.

  4. Diagnosis is based on a history of exposure and the presence of airway and mucous membrane irritation. Symptoms usually occur rapidly after exposure.

    1. Specific levels. Blood levels are not available.

    2. Other useful laboratory studies include arterial blood gases or oximetry, chest radiography, and spirometry or peak expiratory flow rate.

  5. Treatment

    1. Emergency and supportive measures

      1. Remain alert for progressive upper airway edema or obstruction and be prepared to intubate the trachea and assist ventilation if necessary (See Airway and Breathing).

      2. Administer humidified oxygen, treat wheezing with bronchodilators (See Hypoxia), and observe the victim for at least 4–6 hours for development of pulmonary edema (See Hypoxia).

    2. Specific drugs and antidotes. There is no specific antidote.

    3. Decontamination

      1. Inhalation. Remove the victim from exposure and give supplemental oxygen if available.

      2. Skin and eyes. Wash exposed skin and eyes with copious tepid water or saline. Treat frostbite injury as for thermal burns.

    4. Enhanced elimination. There is no role for these procedures.

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