EVALUATION OF ACUTE CASES OF SO2 GAS POISONING DUE TO REACTION OF SODIUM HYDROSULFITE WITH WATER

nasal passages has an immediate neutralizing effect on low concentrations of inhaled SO2 with the formation of sulfite or bisulfate. The metabolic fate of these species is not fully understood though absorbed SO2 is eventually excreted as sulfate (4-9).

Following exposure to 5 ppm SO2, dryness of the nose and throat and a measurable increase in the resistance to bronchial airflow is observed; a decrease in tidal volume occurs at 6-8 ppm. Lacrimation, rhinorrhoea, cough, increased bronchial secretions and bronchoconstriction occur at concentrations exceeding 10-50 ppm. In more severe cases, non-cardiac pulmonary edema and respiratory arrest may supervene. 400-500 ppm is considered to be an immediate danger to life and 1000 ppm can lead to death within 10 min. Corneal and dermal burns can follow exposure to liquefied SO2. Survivors of massive SO2 exposure have shown a chronic obstructive defect in serial pulmonary studies along with bronchial hyper reactivity (10-11).

In present study the symptoms of the upper respiratory tract such as breathlessness, coughing, sore throat and nausea vomiting were seen. Only two patients had conjunctival hyperemia and bronchoconstriction. Non-cardiac pulmonary edema didn't develop in our patients. We could not measure the amount of SO2 in the environment but it was estimated that patients exposed to approximately 20-ppm SO2. Two of the patients exposed to the gases for 30 minutes while the others exposed for nearly one hour but they were working in farther place. The patients applied to the emergency department 30 minutes after the event.

After removal from exposure, symptomatic patients should be assessed at a hospital. Admission for observation and treatment is mandatory in those with persisting symptoms following substantial SO2 exposure. The eyes and skin should be irrigated with water, if irritation is present. Corneal and dermal burns from liquefied SO2 should be treated conventionally and with the involvement of ophthalmic and plastic surgeons respectively. Nebulized salbutamol or other B2 agonist can relieve bronchoconstriction; inhaled corticosteroids may be of value. The role of corticosteroids (inhaled or systemic) in preventing the onset of non-cardiogenic pulmonary edema is uncertain. Mechanical ventilation with positive end-expiratory pressure (PEEP) will be required if non-cardiogenic pulmonary edema ensues (6,10). Oxygen and 200 mg salbutamol mediflexes were administered to the patients applied to the emergency department. In our cases, SO2 gases released from adding water unconsciously to sodium hydrosulfite caused toxic effects by the way of inhalation. It was a fault that the patients hadn't been educated for the reactions. The personnel worked in industrial and textile factories have to be informed about these kinds of chemical reactions. The prevention and first aid and the technical hardware have to be provided.