A42-02 Lipoid Pneumonia Associated With Occupational Exposure to Industrial Coating Materials

Abstract Background Lipoid pneumonia is a rare, underdiagnosed inflammatory lung disease characterized by lipid accumulation in the alveoli. It may be exogenous, due to aspiration or inhalation of lipid-containing substances, or endogenous, secondary to lipid release from degenerating cells. Occupational exposure to volatile organic or oily materials can occasionally lead to exogenous lipoid pneumonia. Case Report A 31-year-old male presented with a two-month history of cough and dizziness. He denied systemic illness or medication use. He was a light smoker (10 pack-years) and had worked for six years in industrial surface coating involving organic solvent-based materials. Physical examination revealed bilateral inspiratory crackles. High-resolution chest CT showed diffuse ground-glass and nodular opacities in all lobes, initially interpreted as atypical pneumonia. Empiric moxifloxacin (400 mg/day) for one week produced no improvement. Autoimmune and infectious workup were unremarkable. To further evaluate the diffuse pulmonary opacities, bronchoscopy with bronchoalveolar lavage (BAL) was performed. Cytologic analysis showed a macrophage-predominant pattern with numerous lipid-laden macrophages staining positive with Oil Red O, confirming alveolar lipid accumulation. No acid-fast bacilli, fungi, or malignant cells were detected, and microbial cultures and PCR were negative for infectious agents. Pulmonary function testing demonstrated FEV1 75%, FVC 76%, and DLCO/VA 71%. The patient received methylprednisolone 16 mg/day for one month and discontinued occupational exposure. After therapy, symptoms resolved, and follow-up testing showed FEV1 87%, FVC 92%, and DLCO/VA 82%. Control imaging demonstrated near-complete regression of radiologic findings. Discussion Exogenous lipoid pneumonia has been described after chronic inhalation or exposure to oily or solvent-based aerosols. It may radiologically mimic infectious or neoplastic processes, often leading to diagnostic delay. In this case, BAL findings played a critical diagnostic role by confirming lipid-laden macrophages and excluding infectious etiologies. The marked clinical and radiologic improvement following corticosteroid therapy and cessation of exposure further supported the diagnosis. Although dizziness is an uncommon symptom, it may reflect systemic absorption of volatile compounds during prolonged occupational exposure. Conclusion Occupational exposure to organic coating agents should be considered among potential causes of exogenous lipoid pneumonia. Early recognition, confirmation with BAL cytology, avoidance of exposure, and corticosteroid therapy can result in significant clinical and radiological improvement. Figure 1. Thoracic CT Images A: Initial HRCT showing diffuse bilateral ground-glass and nodular opacities. B: Follow-up HRCT after corticosteroid therapy and cessation of exposure demonstrating marked regression of findings. This abstract is funded by: none