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Causation Reports

Sulfur Dioxide


Exposure to very low concentrations of sulfur dioxide have been shown to produce definitive effects in exposed individuals. For example: exposure to 0.5 ppm sulfur dioxide for three minutes resulted in increased airway resistance, wheezing, chest tightness, dyspnea, and bronchoconstriction; exposure to from 0.6 to 0.8 ppm for 5 minutes produced increased airway resistance; exposure to 4 ppm for 20 minutes resulted in changes in the defense capabilities of the lung;34 exposure to 5 ppm for 10 minutes resulted in increased airway resistance; exposure to from 1 to 8 ppm for 10 minutes resulted in increased tidal volume, respiratory rate and pulse; exposure to 5 ppm for 10-30 minutes resulted in increased flow resistance after one minute, cough, and irritation. Exposures to from 6 to 12 ppm may cause nasal and throat irritation, to 10 ppm may cause upper respiratory irritation and nosebleeds, to 20 ppm may cause definite eye irritation, chronic respiratory symptoms and exposures in excess of 100 ppm are considered to be an immediate danger to life. Long-term, low-level exposure to sulfur dioxide is also reported to be related to the development of COPD. Asthmatics are particularly susceptible to the effects of sulfur dioxide while healthy non-asthmatics can show pulmonary function changes following inhalation exposures to as little as 1ppm sulfur dioxide.

Animal studies have demonstrated the effects of sulfur dioxide on the nasal mucosa including a progression from normal ciliated epithelium to cuboidal epithelium with complete disappearance of cilia to squamous stratified epithelium. A study in rats exposed to sulfur dioxide produced respiratory mucus cell hyperplasia resulting in hypersecretion of mucus and accumulation of mucus throughout the respiratory tract, a condition similar to that observed in human bronchitis. Mice exposed to sulfur dioxide were reported to exhibit edema, loss of cilia, epithelial thinning and epithelial desquamation in olfactory epithelial tissue. Rabbits exposed to sulfur dioxide were used as models for human bronchitis and exposed dogs showed increased bronchial responsiveness. Hypertrophy and hyperplasia of the submucosal mucous glands in exposed rat tracheas have also been reported. Another study in rats exposed to as little as 5ppm sulfur dioxide demonstrated glutathione depletion in the respiratory tract. Mice exposed to 10 ppm sulfur dioxide for 24 hours showed lesions in the nasomaxillary turbinates (nasal area) consisting of edema, necrosis and desquamation of the respiratory and olfactory epithelium. Another study reported edema, loss of cilia, epithelial thinning and epithelial desquamation in olfactory epithelia of mice exposed to sulfur dioxide. Loss of cilia in response to acute sulfur dioxide exposure appears to constitute the initial injury event which compromises the upper respiratory immune system while at higher concentrations, general exfoliation of the epithelium has been reported in dogs. After long-term exposure to sulfur dioxide, dogs have been reported to exhibit bronchoconstriction, chronic bronchitis and nasopharyngeal changes including epithelial proliferation, loss of secretory material and moderate mononuclear cell infiltration. Mucociliary clearance disruption has been demonstrated in guinea pig tracheas and in exposed ferrets. Also of interest is the initiation of sinusitis in rabbits by exposure to sulfur dioxide and the similar effect noted in humans. Allergic rhinitis in children has been noted to be related to sulfur dioxide concentrations in the atmosphere.

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