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cited a case of an accidental exposure to sulfur dioxide at a high concentration for 15–20 min that led to the development of a severe, irreversible obstructive syndrome (Woodford et al., 1979). The pulmonary effects of accidental exposure to sulfur dioxide appear to be limited to gaseous sulfur dioxide.

An excellent review of studies involving controlled human exposure is available (Greenfield, Attaway and Tyler, 1976). Briefly, the major health effects of exposure to sulfur dioxide at less than 25 ppm (for various durations) are irritation of mucous membranes, throat, esophagus, and eyes; reflex cough; increase in respiratory rate associated with decrease in depth of respiration; decrease in nasal mucus flow; variable effects on tracheal and bronchial mucus flow; decrease in forced expiratory volume and flow; decrease in airway conductance; and increase in airway resistance.

An estimated 10–20% of the population will respond with hyperreactivity on exposure to sulfur dioxide. Koenig et al. (1980) have shown that asthmatic adolescents are more sensitive than healthy nonsmoking adults to sulfur dioxide at 1 ppm. As demonstrated by Lawther et al. (1975), the changes in airway resistance after exposure to sulfur dioxide at less than 30 ppm are short-lived. Greenfield, Attaway and Tyler, (1976) reviewed similar changes after short-term exposures to sulfur dioxide at concentrations greater than 25 ppm.

Another review (EPA, 1982) indicated that recovery to normal functional values can occur in as little as 5 min after acute exposure of normal resting subjects (Lawther et al., 1975), but may take 30–60 min after exposure during exercise (Bates and Hazucha, 1973), after exposure of exercising asthmatic subjects (Sheppard et al., 1981; Koenig et al., 1981), or after exposure of other sensitive subjects (Gokemeijer et al., 1973; Lawther et al., 1975). Weir and Bromberg (1975) suggested that persons with minimal airway disease are probably not more susceptible than normal persons to the effects of sulfur dioxide. However, this latter conclusion is questionable, in that the presence of pre-existing disease in the subjects interfered with attempts to define threshold concentrations of sulfur dioxide. Asthmatic subjects exposed to sulfur dioxide at 5 ppm for 5 min while exercising have had asthmatic attacks (Sheppard et al., 1980).

Epidemiologic data on sulfur dioxide are characteristically difficult to assess, because of the spectrum of pollutants and particles associated with ambient sulfur dioxide. A number of acute air-pollution episodes in this century have been associated with increased mortality. Incidents in the Meuse Valley, Donora (Pennsylvania), London, and New York City have provided evidence that increased pollution has observable effects on human health (Greenfield, Attaway and Tyler, 1976). Retrospective studies of these events have demonstrated that deaths most often occurred among persons over 45 who were already suffering from chronic heart or lung disease; the effects of sulfur dioxide alone were not assessed. Lung-function measurements made daily on four normal subjects and two with bronchitis in London showed that daily variations in lung function were small and were related to respiratory infections (EPA, 1982). Concentrations of sulfur dioxide correlated with variations in peak flow rates and airway resistance. Increased sulfur dioxide pollution has been related to decreases in lung function (FEV1) in children. Several

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