Siderosis is a condition defined by the pathological accumulation of excess iron within the tissues of a specific organ or region of the body. While iron is necessary for life, its presence in abnormally high concentrations can generate toxic free radicals that damage cells. This localized iron deposition distinguishes siderosis from systemic iron overload disorders, such as hereditary hemochromatosis. Siderosis is typically acquired through environmental exposure or trauma, leading to tissue damage that correlates with the concentration and duration of the iron’s presence.
Distinct Forms of Siderosis
Siderosis most frequently applies to two distinct conditions affecting the eyes and the lungs. Ocular siderosis, also known as siderosis bulbi, results from a penetrating injury where a metallic, iron-containing foreign body becomes lodged inside the eye. Common causes include high-velocity trauma from hammering, grinding, or welding, causing a microscopic fragment to perforate the globe. The retained fragment slowly dissolves, and the iron ions diffuse into surrounding ocular structures, including the lens, iris, and retina. This iron-induced toxicity progressively damages the delicate light-sensitive cells of the retina.
Pulmonary siderosis, or Welder’s Siderosis, is an occupational disease occurring after the chronic inhalation of iron oxide dust or fumes. Workers in environments like welding, mining, and foundry work are at risk of inhaling fine iron particles over many years. These particles are subsequently engulfed by immune cells called macrophages within the lung parenchyma, leading to iron accumulation. This condition is a form of pneumoconiosis, but it is often considered “benign” because the iron oxide is typically inert. It does not cause the extensive scarring or fibrosis seen with other inhaled materials like silica or asbestos, though it can still cause radiographic changes.
Identifying Symptoms
The clinical presentation of siderosis depends on the location of the iron deposition, reflecting organ dysfunction. Ocular siderosis is characterized by a gradual decline in visual function, often presenting as night blindness or difficulty seeing in low light. Iron accumulation can cause noticeable physical changes, such as a change in the iris color, known as heterochromia, where the iris darkens to a rusty brown hue. Additionally, the pupil may become permanently fixed and dilated, and a rust-colored cataract may form on the lens.
Symptoms of pulmonary siderosis are often mild or entirely absent for many years, reflecting the non-scarring nature of the deposits. When symptoms occur, they are generally related to the respiratory system and may include a persistent cough or chest unease. Some individuals may experience mild shortness of breath, particularly during physical exertion. These symptoms are more likely if the iron exposure is accompanied by other irritants, such as silica, which can induce scarring and lead to siderosilicosis.
Diagnostic Procedures and Management
Diagnosis relies on patient history, physical examination, and specialized imaging or functional tests tailored to the affected organ. For ocular siderosis, a detailed ophthalmological examination using a slit lamp can reveal rust-colored deposits in the anterior structures of the eye. Functional assessment uses an electroretinogram (ERG), which measures the electrical responses of the retina and often shows a characteristic reduction in the b-wave amplitude due to toxicity. Imaging techniques like computed tomography (CT) or high-frequency ultrasonography are used to accurately locate the retained iron-containing foreign body.
For pulmonary siderosis, chest X-rays or high-resolution CT scans are used to identify the condition. These images typically show characteristic small, dense nodular opacities scattered throughout the lungs, representing the accumulated iron particles. For ocular siderosis, the immediate surgical removal of the foreign body is the mainstay of treatment. Timely removal, often using pars plana vitrectomy or magnetic extraction, is necessary to halt the diffusion of toxic iron ions and prevent irreversible vision loss.
Since pulmonary siderosis is often benign, the primary management involves removing the patient from the source of iron oxide exposure to prevent further accumulation. Specific treatments for the iron deposition itself are limited, and the condition is mostly monitored with serial imaging. Aggressive treatments, such as corticosteroids, are reserved for distinct, non-occupational forms of pulmonary iron accumulation, like Idiopathic Pulmonary Hemosiderosis, which involves recurrent bleeding and leads to lung tissue damage.