Abstract
Welder's pneumoconiosis, which is caused by the inhalation of welding fumes, is one of the major pneumoconioses in Japan. The major component of welding fumes is iron oxide. Although welder's pneumoconiosis has been considered to be inert, recent reports revealed the possibility of developing fibrosis. In this article, we demonstrate radiological and pathological features of welder's pneumoconiosis, and also review the mechanisms of developing pulmonary fibrosis. In high-resolution CT (HRCT), typical welder's pneumoconiosis shows fine centrilobular nodules in both lung fields. In some cases, fibrotic changes may be seen in subpleural areas in both lower lung fields. Lung biopsy specimens show numerous hemosiderin-laden macrophages within alveolar spaces associated with mild to moderate interstitial fibrosis. The mechanisms of developing fibrosis can be explained by “overload phenomenon”. Namely, in cases of mild exposure to welding fumes, iron oxides and hemosiderin-laden macrophages locate within air-spaces and may be reduced in numbers by mucociliary transport system. However, in cases of massive inhalation, accumulation of iron oxides and hemosiderin-laden macrophages exceed the capacity of mucociliary transport system. As a result, they invade into the interstitium and cause interstitial inflammation or thickening and eventually pulmonary fibrosis.
