Metal fume fever is a clinical syndrome most commonly caused by occupational exposure to fumes that contain metal, generated by welding and related processes. Polymer fume fever is clinically similar to metal fume fever but is caused by exposure to specific fluorinated polymer products, such as polytetrafluoroethylene (PTFE, known as Teflon®). Diagnosis is by clinical evaluation. Treatment is supportive.
Metal fume fever was first recognized in the 1800s in association with zinc fume and the pouring of molten brass. In the 1970s, metal fume fever was fairly common among welders; 31% of welders aged 20 to 59 years had a least one episode during their career. In the US, improvements in safety regulations and workplace exposure controls have made metal fume fever less common today; now, an estimated 1500 to 2500 cases occur annually in the US.
Metal fume fever may also affect welders in nonoccupational settings, such as artists or hobbyists. The most common type of metal implicated in metal fume fever is zinc, although other metals have been suggested as potential causes in case reports.
Metal fume fever is distinct from cadmium pneumonitis, a more severe syndrome associated with hypoxia and respiratory failure.
Polymer fume fever is clinically similar to metal fume fever but is caused by exposure to fumes generated when polytetrafluoroethylene (Teflon®) is heated to > 300° C. Polymer fume fever was first reported in 1951 in a case series of workers handling PTFE at elevated temperatures.
In the US, improvements in workplace hygiene have decreased the incidence of occupational polymer fume fever. Exposure to PTFE fume due to overheating of Teflon® cookware in home kitchens has resulted in polymer fume fever in people and has been fatal to pet birds.
Pathophysiology
Symptoms and Signs
Metal fume fever typically manifests with nonspecific symptoms that mimic influenza (eg, fever, shaking chills, malaise, myalgias, arthralgias, headache). Other symptoms may include dry cough, pleuritic chest pain, shortness of breath, pharyngitis, muscle cramping, and abnormal taste sensation. Abdominal pain, nausea, and vomiting are less common.
Onset of symptoms is delayed for 4 to 10 hours after exposure; symptoms may occur after the worker has completed a shift, making the association between symptoms and occupational exposure more difficult to identify.
Tachyphylaxis may occur when exposure is repeated. As a result, symptoms lessen over the course of the work week but become more severe after a weekend hiatus; it is thus sometimes called Monday morning fever.
Severe metal fume fever is rare and mimics acute respiratory distress syndrome (ARDS), causing fever, hypoxia, and tachypnea.
Symptoms of polymer fume fever are the same as those of metal fume fever, so a history of known exposures is needed to differentiate the two syndromes. However, polymer fume fever does not cause tachyphylaxis.
Diagnosis
Clinical evaluation
Chest x-ray
ECG
There are no definitive diagnostic tests for metal fume fever; diagnosis relies largely on history and physical examination. Metal fume fever is diagnosed when workers or others with a history of exposure to zinc fume (eg, welders) present with the characteristic symptoms of the syndrome. Because the symptoms are similar to influenza symptoms, an occupational or exposure history is necessary to avoid a delay in diagnosis.
The most common objective findings are fever and sinus tachycardia. Other findings are typically more subjective and may include rigors and diaphoresis. Pulmonary examination is typically normal with normal respiratory rate, effort, and chest wall excursion; rales or wheezing is occasionally heard.
When metal fume fever is severe, pulmonary examination detects respiratory distress, wheezes, rales, and/or rhonchi. Because severe metal fume fever is rare, alternative diagnoses (eg, cadmium pneumonitis, other causes of ARDS) should be considered.
Chest x-rays are typically normal in metal fume fever but help differentiate metal fume fever from other causes of similar symptoms, such as pneumonia. Mild vascular congestion may be present but is nonspecific. When metal fume fever is severe, chest x-rays show diffuse bilateral patchy infiltrates, as occur in ARDS. CT of the chest, if done, typically shows bilateral mild atelectasis and pleural effusion. In severe cases, CT may show bilateral diffuse alveolar or ground-glass opacities.
Laboratory tests, if done, may detect nonspecific leukocytosis with a left shift. Inflammatory markers (eg, erythrocyte sedimentation rate, C-reactive protein) may be elevated. In case reports, serum zinc levels were elevated during acute episodes, but this testing is not available in the acute care setting and therefore is of little clinical use.
Pulmonary test results, usually not needed immediately, may be normal or indicate slightly decreased vital capacity, which resolves when symptoms resolve. In severe cases, a restrictive lung disease pattern may be present.
Diagnosis of pulmonary fume fever is also clinical; it is based on a history of occupational exposure to heated PTFE or to overheated Teflon® cookware, followed by the onset of the characteristic symptoms of this syndrome. The characteristic symptoms and signs and diagnostic testing results are the same as those for metal fume fever, except polymer fume fever does not cause tachyphylaxis.
Prognosis
Metal fume fever is a benign disorder that resolves spontaneously over 12 to 48 hours after the last exposure to zinc or other metal fumes; however, tachyphylaxis may occur if exposure is repeated. Severe cases that manifest with ARDS-like symptoms may require supportive measures for days to weeks. In case reports, repeated episodes can result in chronic obstructive pulmonary disease (COPD), occupational asthma, or pulmonary fibrosis.
The prognosis in polymer fume fever is similar to that in metal fume fever.
Treatment
Symptom relief, including antipyretics and nonsteroidal anti-inflammatory drugs (NSAIDs)
For severe respiratory distress, mechanical ventilation
Treatment of metal fume fever and polymer fume fever is supportive and may include antipyretics, NSAIDs, and other symptomatic measures. Patients are often referred to the emergency department, but most of those patients can be discharged home. Oral or IV corticosteroids are not recommended because they have not shown efficacy in the setting of metal fume fever. Rarely, patients with preexisting lung disease (eg, asthma, chronic obstructive pulmonary disease) require treatment and inpatient admission for exacerbation of the preexisting disease. If severe cases of either syndrome cause respiratory distress, the same treatments used for ARDS (eg, mechanical ventilation, positive end-expiratory pressure [PEEP]) are indicated.
Prevention
Workers with metal fume fever should be cautioned to minimize exposure to zinc fumes by using personal protective equipment (PPE). Contacting the employer to implement other workplace exposure controls (elimination, substitution, engineering controls, administrative controls) is indicated if PPE is inadequate to control exposure or if multiple workers are affected.
Key Points
Zinc is the primary metal associated with metal fume fever, but other metals may be involved.
Occupational exposure to zinc fumes, as may occur during welding, may result in metal fume fever.
Polymer fume fever is a similar syndrome but results from exposure to heated tetrafluoroethylene (Teflon®) or overheated Teflon® cookware.
Metal fume fever typically results in flu-like symptoms; a history of exposure is necessary to differentiate it from influenza and other disorders.
Most testing yields nonspecific findings, but chest x-ray can help differentiate metal fume fever from some other disorders.
Treat supportively (eg, with antipyretics and NSAIDs for mild symptoms).
In metal fume fever, symptoms resolve within 12 to 48 hours after cessation of exposure; caution workers to minimize future workplace exposure to metal fumes.
