Mechanism of action—At room temperature, the solubility of SO2 is approximately 200 g SO2/L of water. Because of its high solubility, when SO2 contacts moist membranes, it transiently forms sulfurous acid. This acid has severe irritant effects on the eyes, mucous membranes, and skin. Approximately 90% of inhaled SO2 is absorbed in the upper respiratory tract, the site of its principal effect. The inhalation of SO2 causes bronchial constriction and produces profuse bronchorrhea; parasympathetic reflexes and altered smooth muscle tone appear to be involved. The clinical outcome is an acute irritant asthma. Exposure to 5 ppm SO2 for 10 minutes leads to increased resistance to airflow in most humans. Exposures of 5–10 ppm are reported to cause severe bronchospasm; 10–20% of the healthy young adult population is estimated to be reactive to even lower concentrations. The phenomenon of adaptation to irritating concentrations has been reported in workers. However, current studies have not confirmed this phenomenon. Asthmatic individuals are especially sensitive to SO2.
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Clinical effects and treatment—The signs and symptoms of intoxication include irritation of the eyes, nose, and throat, reflex bronchoconstriction, and increased bronchial secretions. In asthmatic subjects, exposure to SO2 may result in an acute asthmatic episode. If severe exposure has occurred, delayed-onset pulmonary edema may be observed. Cumulative effects from chronic low-level exposure to SO2 are not striking, particularly in humans, but these effects have been associated with aggravation of chronic cardiopulmonary disease. When combined exposure to high respirable particulate loads and SO2 occurs, the mixed irritant load may increase the toxic respiratory response. Treatment is not specific for SO2 but depends on therapeutic maneuvers used to treat irritation of the respiratory tract and asthma. In some severely polluted urban air basins, elevated SO2 concentrations combined with elevated particulate loads has led to air pollution emergencies and a marked increase in cases of acute asthmatic bronchitis. Children and the elderly seem to be at greatest risk. The principal source of urban SO2 is the burning of coal, both for domestic heating and in coal-fired power plants. High-sulfur transportation fuels also contribute. Both also contribute to the respirable fine particulate load and to increased urban cardiorespiratory morbidity and mortality.
Nitrogen dioxide (NO2) is a brownish irritant gas sometimes associated with fires. It is formed also from fresh silage; exposure of farmers to NO2 in the confines of a silo can lead to silo-filler’s disease, a severe and potentially lethal form of acute respiratory distress syndrome. The disorder is uncommon today. Miners who are regularly exposed to diesel equipment exhaust have been particularly affected by nitrogen oxide emissions with serious respiratory effects. Today, the most common source of human exposure to oxides of nitrogen, including NO2, is automobile and truck traffic emissions. Recent air pollution inventories in cities with high traffic congestion have demonstrated the important role that internal combustion engines have in the increasing NO2 urban air pollution. A variety of disorders of the respiratory system, cardiovascular system, and other problems have been linked to NO2 exposure.
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