Metal fume fever is an acutely noxious inhalation syndrome secondary to metal oxide fumes. Despite preventative strategies sporadic cases are likely to continue to present to emergency departments.
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A 55 year old man presented to the emergency department at 9 pm. He complained of feeling generally unwell for the previous five hours. He described malaise, fatigue, cough, fever, nausea, and dyspnoea at rest. He had no previous medical history of note and was usually fit and well. He was a non-smoker. He worked as a plumber and on the day of admission had been using an oxyacetylene torch to remove a steel tank.
On examination, he was unable to talk in full sentences. His respiratory rate was 24/min with an oxygen saturation of 94% in room air. Chest examination was normal. His pulse rate was 100/min and he was feverish at 39°C. There were no other findings of note. Blood gas analysis demonstrated acute type I respiratory failure with an arterial oxygen partial pressure of 8.8 kPa. There was a neutrophil leucocytosis but no other abnormality of baseline pathology. A chest radiograph revealed patchy opacification in the right perihilar area.
His 18 year old son, who had been working with him all day, presented to the emergency department simultaneously. He complained of malaise, nausea, vomiting, and cough. He had no previous medical history. Examination and investigation were unremarkable.
A further coworker presented to a local minor injury unit the same night with similar symptoms to the 18 year old patient. He required no medical intervention.
A diagnosis of metal fume fever was made and the 55 year old man admitted for observation and oxygen therapy. His son was discharged. By the following morning both had made a full recovery.
Metal fume fever (MFF)—“brass founders ague”, “zinc shakes”, “Monday morning fever”—is a self limiting inhalation fever attributed to a number of metal oxide fumes. The history is characterised by fever, headache, myalgia, fatigue, and dyspnoea. Other features include cough, thirst, a metallic taste, salivation, and a neutrophil leucocytosis. Radiography may demonstrate bilateral diffuse infiltrative pulmonary lesions. Pulmonary function tests demonstrate a significant reduction in vital capacity, transfer factor and arterial oxygen partial pressure. Urine and plasma metal levels may be increased.
Onset is typically rapid, occurring between three and 10 hours after exposure. Spontaneous recovery occurs within 24 hours. No long term complications are known.1
MFF is classically associated with zinc oxide fume exposure from welding galvanised steel or brass. It is also seen in association with high temperature zinc coating processes and metal pouring in brass foundries. Magnesium and copper oxide fumes are more rarely the causative agents. Approximately 2000 cases are reported annually in the United States.2,3
The pathophysiology is unclear but seems to reflect a direct toxic effect. The lack of a latent period and the fact that large proportions of a single workforce can be affected are against an immunological basis for the disease. 4 There is evidence of an exposure dependent neutrophil alveolitis in association with tumour necrosis factor α, interleukin 6, and interleukin 8 cytokine release from pulmonary cells.4 Interestingly there is evidence of rapid adaptation after repeated exposure though the transient nature of this tolerance is reflected in the synonym “Monday morning fever”. It has been postulated that tolerance occurs because of induction of metallothionein protein synthesis. These proteins bind to heavy metals preventing toxic metal accumulation. 5
Diagnosis is based on clinical suspicion, clinical findings, and rapid resolution. Evidence of possible exposure is critical. Treatment is symptomatic. The syndrome needs to be differentiated from serious MFF seen after military smoke exposure, which typically has a biphasic response with severe relapse 24 to 48 hours after initial remission.6 It should also be differentiated from true chemical pneumonitis after metal fume exposure. This is particularly associated with cadmium fumes but also occurs with manganese, mercury, and nickel. In the early stages, it may be indistinguishable from MFF but the pneumonitis is progressive and usually complicated by non-cardiogenic pulmonary oedema. Cadmium also injures the renal tubules resulting in acute renal dysfunction.1
Preventative strategies for MFF are aimed at reducing fume exposure concentrations.7 “Toxic” levels have not been established. However, Fine et al have demonstrated that inhalation of traditionally safe levels of zinc oxide can produce MFF symptoms and a rise in plasma interleukin 6.8 In the UK, the Reporting of Injuries, Diseases and Dangerous Occurrence Regulations (1995) place responsibility on employers to report MFF to the Health and Safety Executive once it has been diagnosed in writing by a doctor.7
MFF is a common, acute, severe occupational syndrome. Despite preventative strategies, sporadic cases continue to present to emergency departments. Recognition of the possibility of an inhalation syndrome requires an understanding of the aetiology and an adequate occupational history. Early recognition can prompt a more directed management approach and permit the exclusion of more serious inhalational syndromes.
PK and HY were responsible for the diagnosis and management of the case, reviewed the literature and wrote the paper. IOS reviewed and advised on the paper and is the guarantor for the paper.
Conflicts of interest: none.
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