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What is involved? (including coding of cases) SABRE Case Studies and Information
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Toxic inhalations at a blast furnace
At a large steel manufacturing plant in NSW, fourteen workers developed acute respiratory symptoms while clearing hot air inlets after a temporary cool down in a blast furnace. Workers were opening the inlets to the furnace using a long steel rod, allowing small quantities of blast furnace gas at high pressure and temperature to escape into their breathing zones. Despite respiratory protection, 3 separate incidents occurred with workers noticing an identical illness. About 15-20 minutes after exposure, workers noticed chest tightness on inspiration accompanied by dyspnoea, sweating and rigors. Three workers were sent to hospital for assessment. Chest X rays showed pulmonary infiltrates compatible with acute pulmonary oedema, and spirometry demonstrated lung restriction, while oximetry showed low saturations. All workers recovered completely, although the two workers worse affected took some weeks to get back to normal. Extensive occupational hygiene sampling, correlated with clinical findings, demonstrated the most likely cause to be inhalation of nitrogen oxides at high pressure. Nitrogen oxides (NOx) occur in blast furnace gas in high levels (up to 1000 ppm), and are generated in particular under conditions of cooling. Nitrogen oxides and in particular nitric oxide have been implicated in the production of furnace “cracking” which contributes to blast furnace dysfunction. Nitric oxide is a colourless, odourless gas, which rapidly oxidises in air to nitrogen dioxide, a reddish-brown gas with a pungent odour, and dinitrogen tetroxide. SABRE doctors will recognise NOx as the cause of “silo-filler’s disease”, where generation of nitric oxide, nitrogen dioxide and dinitrogen tetroxide fumes occurs during the fermentation of vegetable matter in a confined area. The unwary farmer may be overcome by fumes and succumb while trapped inside the silo. However, toxicity in silo-filler’s disease is primarily due to nitrogen dioxide, whereas in this case the toxicity is more likely to have been due to a mixture of nitric oxide (NO) and nitrogen dioxide. With inhalation of high concentrations of NOx, acute pulmonary oedema is well described, after initial symptoms of throat irritation, cough, headache, a sensation of chest tightness, chills and fevers, which usually pass off within 30 minutes. Delayed pulmonary oedema may then occur, as in this case, usually followed by an uneventful recovery. Exposure to low levels of NOx (4-24 ppm) may result in the above symptoms, while fatal pulmonary oedema may occur with levels of 100-150 ppm. The long term consequences of “cold blast furnace syndrome” are difficult to predict. Acute inhalational exposures have been associated with the development of reactive airways dysfunction syndrome, irritant-induced asthma, pulmonary fibrosis, and obliterative bronchiolitis, but at reassessment one year after the event, no worker had any residual abnormality. Engineering controls and further respiratory protection were implemented, and appear to have controlled the hazard. This “cold blast furnace syndrome” represents a new hazard of blast furnace work and should be considered with respiratory injuries in blast furnace workers.
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