Case presentation
A 66-year-old Caucasian man was referred to the outpatient clinic with a 2-year history of exertional breathlessness. He had no other respiratory symptoms, had never smoked and was not aware of any previous asbestos exposure. He was not on any medication and had no allergies. He had worked as an engineer for 20 years where he did a significant amount of welding but always wore a face shield. A review of systems was unremarkable.

On examination, he was not clubbed or cyanosed, and his chest was clear to auscultation. Pulmonary function tests showed a moderately severe obstructive defect, gas trapping and a significantly reduced gas transfer factor: forced expiratory volume in 1 second (FEV1) 1.58 (49.1%); vital capacity (VC) maximum 3.0 (75.9%); FEV1/VC maximum 52.6%; total lung capacity (TLC) 7.2 (100%); residual volume (RV) 4.3 (157%); RV/TLC ratio 140.3%; carbon monoxide transfer factor 3.57 (44.0%); carbon monoxide transfer coefficient 0.77 (66.8%). His resting oxygen saturations were 95% on room air; however, he desaturated to 89% after 4 minutes of walking, which was associated with a peak modified Borg score (perceived breathlessness score) of three, indicating moderate breathlessness. A chest radiograph showed diffuse generalised reticular nodular shadowing with a suggestion of enlarged hila (Figure 1a). Computed tomography scanning revealed multiple small nodular opacities throughout both lungs, predominantly in the mid and upper zones (Figure 1b). Transbronchial biopsies were non-diagnostic, therefore video-assisted thoracoscopic lung biopsy was performed. Microscopic examination of these specimens showed marked deposition of coarse iron granules in a centrilobular distribution, with foci of associated fibrosis (Figures 2 and 3). The appearances were consistent with pulmonary siderosis most likely related to his occupational welding history. In 3 years of follow-up his lung function and chest radiograph have not progressed.

Discussion
Inhalation of iron compounds occurs commonly in paint factories, during welding and steelmaking, and at various stages of iron mining and iron refining. Doig and McLaughlin first described 'welders' siderosis' in 1936 when they carried out a prospective study examining the clinical and chest radiological characteristics of 16 electric arc welders [1]. All but one of these original subjects were followed for 9 years: four of these demonstrated progressive radiographic reticular changes, nine showed no radiographic changes, and in two men (both of whom had spent significantly less time welding), there was evidence of at least partial resolution of the initial radiographic opacities [3]. All subjects, however, remained in good health, leading to the conclusion that siderosis (in its pure form) was not associated with respiratory symptoms or functional impairment. This view was supported by subsequent pathological investigations of the lungs of subjects occupationally exposed to iron oxide fumes, which did not demonstrate any evidence of pulmonary fibrosis [3]. As a result, the apparently inert nature of iron compounds led to the classification of pulmonary siderosis as a 'benign pneumoconiosis' [2].