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38-year-old man presented to the pulmonary clinic with a 9-month history of progressive bandlike burning pain around his chest and sharp stabbing pain anteriorly, along with shortness of breath. He had been a welder for 15 years, making iron dumpsters in a plant. He noticed shortness of breath when climbing stairs and moderate symptoms when walking. He also reported a dry cough. He denied any other systemic symptom and had no other medical or
surgical history. He was a nonsmoker.
38-year-old man presented to the pulmonary clinic with a 9-month history of progressive bandlike burning pain around his chest and sharp stabbing pain anteriorly, along with shortness of breath. He had been a welder for 15 years, making iron dumpsters in a plant. He noticed shortness of breath when climbing stairs and moderate symptoms when walking. He also reported a dry cough. He denied any other systemic symptom and had no other medical or
surgical history. He was a nonsmoker.
38-year-old man presented to the pulmonary clinic with a 9-month history of progressive bandlike burning pain around his chest and sharp stabbing pain anteriorly, along with shortness of breath. He had been a welder for 15 years, making iron dumpsters in a plant. He noticed shortness of breath when climbing stairs and moderate symptoms when walking. He also reported a dry cough. He denied any other systemic symptom and had no other medical or
surgical history. He was a nonsmoker.
Ariel Modrykamien, MD; Howard Christie, PA-C; Carol Farver, MD; and Rendell W. Ashton, MD, FCCP (CHEST 2009; 136:310313) A 38-year-old man presented to the pulmonary clinic with a 9-month history of progressive bandlike burning pain around his chest and sharp stabbing pain anteriorly, along with shortness of breath. He had been a welder for 15 years, making iron dumpsters in a plant. He noticed shortness of breath when climbing stairs and moderate symptoms when walking. He also reported a dry cough. He denied any other systemic symptom and had no other medical or surgical history. He was a nonsmoker. Physical Examination His vital signs were as follows: BP, 150/100 mm Hg; heart rate, 78 beats/min; respiratory rate, 14 breaths/ min; temperature, 98.3F; and arterial oxygen satura- tion, 98% while breathing room air. His physical exam- ination was normal except for Velcro-type crackles in both lung bases. Laboratory Findings Laboratory values at presentation showed a hemat- ocrit of 50.4% with a hemoglobin concentration of 16.8 g/dL. Ferritin level was 1,634 ng/mL (normal range, 18 to 300 ng/mL), and iron level was 169 g/dL (normal range, 30 to 140 g/dL). Transferrin saturation was 62% (normal range, 11 to 46%). The patient had a normal WBC and platelet count. His coagulation stud- ies, liver function test, and kidney function test findings were within normal limits. Blood glucose levels and urinalysis findings were normal as well. Pulmonary function tests revealed an FEV 1 /FVC ratio of 76%, an FEV 1 of 78% predicted, and an FVC of 85% predicted. Diffusing capacity of the lung for carbon monoxide was 73% predicted, and diffusing capacity of the lung for carbon monoxide corrected for his alveolar ventilation was 105% predicted. A bronchoscopy was performed showing a normal airway. A bronchial washing and transbronchial bi- opsies of the right middle lobe revealed abundant hemosiderin-laden macrophages. Cultures for bacte- rial and fungal infections, viruses, and AFB were all negative. Serum markers for autoimmune diseases, such as antinuclear antibody, rheumatoid factor, SM, RNP, SSA, SSB, centromere, scleroderma IgG, and Jo-1 antibodies, were negative. Markers for vasculitides, such as cytoplasmic antineutrophil cytoplasmic antibody, perinuclear antineutrophil cytoplasmic antibody, and glo- merular basement membrane antibody, were negative as well. The patient underwent a video-assisted thoraco- scopic surgery with right upper, middle, and lower lobe wedge biopsies (Fig 1, 2) due to the lack of diagnosis. From the Respiratory Institute (Drs. Modrykamien and Ashton, and Mr. Christie) and Department of Anatomic Pathology (Dr. Farver), Cleveland Clinic, Cleveland, OH. The authors have no conflicts of interest to disclose. Manuscript received December 15, 2008; revision accepted December 31, 2008. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal. org/site/misc/reprints.xhtml). Correspondence to: Ariel Modrykamien, MD, Respiratory Insti- tute, A90, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH 44195; e-mail: modryka@ccf.org DOI: 10.1378/chest.08-2954 Figure 1. Pulmonary parenchyma with diffuse brown pigment involving 70 to 80% of thoracoscopic biopsy, centered around the small airways (hematoxylin-eosin, original 12.5). CHEST Postgraduate Education Corner PULMONARY AND CRITICAL CARE PEARLS 310 Postgraduate Education Corner Downloaded From: http://journal.publications.chestnet.org/ on 08/15/2014 Radiology Findings Chest radiography was normal, and a high-resolution CT scan of the chest showed bilateral diffuse centri- lobular ground-glass nodular opacities (Fig 3). What is the diagnosis? Figure 2. Brown hemosiderin pigment is present predominantly within alveolar macrophages surrounding the bronchovascular area of the biopsy (hematoxylin-eosin, original 200). Figure 3. CT scan of the chest showing diffuse centrilobular ground-glass nodular opacities. www.chestjournal.org CHEST / 136 / 1 / JULY, 2009 311 Downloaded From: http://journal.publications.chestnet.org/ on 08/15/2014 Diagnosis: Welders siderosis (pneumoconiosis siderotica) Discussion Welders siderosis or pneumoconiosis siderotica was originally characterized by Doig and McLaugh- lin as a lung disease caused by the inhalation of iron dust. In their report, the authors described 16 electric arc welders who remained in a good state of health despite the diagnosis of siderosis. They con- cluded that this entity was not associated with respi- ratory symptoms or functional impairment. Pneumoconiosis can be classified as fibrotic or nonfibrotic, depending on the presence of fibrosis in the lung biopsy specimen. Fibrotic pneumoconioses usually present with symptoms such as cough and dyspnea, differentiating it from nonfibrotic forms. Silicosis, coal worker pneumoconiosis, asbestosis, talcosis, and berylliosis are examples of fibrotic pneu- moconiosis, whereas baritosis, stannosis, and sidero- sis are nonfibrotic forms. Welding involves mixtures of metals such as iron, manganese, silica, chromium, nickel, and others. In situations where the ventilation is poor or the weld- ing activity is performed in confined spaces, the probability for the development of lung disease increases. The acquired disease depends on the specific fume exposure, the coating of the rods, the welding operation performed, and the metal welded. Therefore, it is essential to distinguish welders pneumoconiosis, which refers to the effect of inhal- ing heterogeneous dusts generated by welding, from welders siderosis, which is the effect of inhaled iron oxide particles alone. Environmental levels of fumes and particles are thought to be directly related to the development of lung disease. Hence the Occupational Safety and Health Administration of the US Department of Labor updated the permissible exposure limit estab- lished for welding fumes to 5 mg/m 3 . However, despite this updated regulation, there are still reports of acute lung diseases in welders exposed to levels as low as 4.3 mg/m 3 . Because welders siderosis is a nonfibrotic pneu- moconiosis, it was originally thought not to be associated with respiratory symptoms. Neverthe- less, some authors described symptomatic disease with interstitial fibrosis in arc welders. It is thought that these cases might have occurred secondary to concomitant inhalation of silicates and iron (silicosiderosis). Some reports have described the occurrence of welders siderosis associated with systemic iron over- load. Three cases of welders siderosis with elevated ferritin, serum iron level, and serum transferring saturation have been reported. None of these pa- tients had hemochromatosis, thalassemia, or sider- oblastic anemia, and there was no history of multiple blood transfusions, iron ingestion, or alcohol con- sumption. The authors concluded that iron overload seemed likely to be due to occupational exposure. Chest CT imaging in patients with pneumoconio- sis siderotica demonstrates small nodules that are more prominent in the middle third of the lung. These nodules indicate radiopaque accumulation of iron particles in macrophages aggregated along the peribronchovascular bundle. These changes are usu- ally reversible and may completely resolve after cessation of exposure. It is important to differentiate welders siderosis from two other entities: idiopathic pulmonary hemo- siderosis and metal fume fever. Idiopathic pulmonary hemosiderosis is a rare in- terstitial lung disease of unknown etiology that oc- curs preferentially in children. Its clinical presenta- tion varies from an acute and fulminant form with diffuse alveolar hemorrhage to a more subacute presentation with cough, dyspnea, repetitive hemop- tysis, and anemia. Sputum and BAL fluid examina- tion show multiple hemosiderin-laden macrophages, and the lung biopsy confirms a bland alveolar hem- orrhage with variables degrees of fibrosis. Metal fume fever, or Monday morning fever, is a self- limiting inhalation fever attributed to a number of metal oxide fumes. It presents with fever, headache, fatigue, and dyspnea within 3 to 10 h after the exposure to heated metals, including galvanized steel, zinc oxide, magnesium oxide, and chromium. Its diagnosis is based on clinical suspicion, and preventive strategies are aimed at reducing fume exposure. Clinical Course Our patient with welders siderosis presented with symptoms of chest pain, severe shortness of breath, and cough. Although patients with nonfibrotic pneu- moconiosis usually present without respiratory symp- toms, on occasion, they may be symptomatic. The presence of iron overload was thought to be related to the inhalation of iron dust because he did not have a history for other sources of endogenous or exoge- nous iron overload. We recommended the patient to wear respiratory protection (respirator) and encour- aged him to work in areas with an effective ventila- tion system. We also recommended that all welders in his plant be screened for serum ferritin, total iron level, and iron binding capacity. 312 Postgraduate Education Corner Downloaded From: http://journal.publications.chestnet.org/ on 08/15/2014 Clinical Pearls 1. Welders siderosis is a nonfibrotic pneumoconi- osis caused by the inhalation of iron dust. 2. Pneumoconiosis siderotica is typically, but not always, asymptomatic. 3. Iron overload can complicate the presentation of this entity. It is important to exclude hemochroma- tosis, thalassemia, sideroblastic anemia, multiple blood transfusions, iron ingestion, and alcohol con- sumption in this clinical scenario. 4. Chest CT imaging shows diffuse, centrilobular, ground-glass, nodular densities. 5. Pathologic changes are reversible, and complete resolution is possible following cessation of exposure. Suggested Readings Doig AT, McLaughlin AI. Clearing of x-ray shadows in welders siderosis. Lancet 1948; 1:789791 Guidotti TL, Abraham JL, DeNee PB, et al. Arc welders pneumoconiosis: application of advanced scanning electron microscopy. Arch Environ Health 1978; 33:117124 Barbee JY Jr, Prince TS. Acute respiratory distress syndrome in a welder exposed to metal fumes. South Med J 1999; 92:510512 Kaye P, Young H, OSullivan I. Metal fume fever: a case report and review of the literature. Emerg Med J 2002; 19: 268269 Doherty MJ, Healy M, Richardson SG, et al. Total body iron overload in welders siderosis. Occup Environ Med 2004; 61:8285 Fidan F, Esme H, Unlu M, et al. Welders lung associated with pneumothorax. J Thorac Imaging 2005; 20:120122 Ioachimescu OC, Farver C, Stoller JK. Hemoptysis in a 77-year-old male with a systolic murmur. Chest 2005; 128:10221027 Chong S, Lee KS, Chung MJ, et al. Pneumoconiosis: comparison of imaging and pathologic findings. Radiographics 2006; 26: 5977 McCormick LM, Goddard M, Mahadeva R. Pulmonary fibrosis secondary to siderosis causing symptomatic respiratory disease: a case report. J Med Case Reports 2008; 2:257 www.chestjournal.org CHEST / 136 / 1 / JULY, 2009 313 Downloaded From: http://journal.publications.chestnet.org/ on 08/15/2014
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