Abstract Introduction Sarcoidosis is a multisystem granulomatous disease characterized by immune-mediated granuloma formation, most commonly affecting the lungs. Environmental triggers, including infectious, organic, and inorganic antigens, have been implicated in its pathogenesis. While many patients achieve remission, up to 20% progress to pulmonary fibrosis as granulomatous inflammation transitions to irreversible parenchymal remodeling. We present the case of a 34-year-old man with significant biomass fuel exposure who developed granulomatous lung disease with fibrosis and pulmonary hypertension, consistent with sarcoidosis secondary to chronic inhalational exposure. Case Description A 34-year-old man recently migrated from Honduras with a history of chronic biomass fuel exposure and previously diagnosed granulomatous lung disease with upper-lobe fibrosis presented with acute hypoxic respiratory failure. He was agitated and profoundly hypoxemic (SpO2 60s), requiring BiPAP followed by intubation. Laboratory studies showed leukocytosis (13.1 K/µL), mixed respiratory acidosis (pH 7.18/PCO2 84/HCO3 31.3), lactic acidosis (4.2 mmol/L), and elevated inflammatory markers. Thoracentesis yielded a transudative effusion without cellular predominance. Infectious and autoimmune workups, including Quantiferon-TB Gold, were negative. Imaging demonstrated upper-lobe-predominant fibrosis consistent with sarcoidosis secondary to chronic inhalational exposure. Transbronchial biopsy revealed non-necrotizing granulomas, and bronchoalveolar lavage was negative for infection. Pulmonary function testing showed obstruction without bronchodilator response and borderline restriction. Echocardiography demonstrated right ventricular hypertrophy and cor pulmonale (RVEF 34%), with precapillary pulmonary hypertension confirmed on right heart catheterization. His condition improved with corticosteroids, diuretics, and sildenafil, allowing discharge on prednisone and Pneumocystis jirovecii prophylaxis without oxygen. He subsequently experienced several readmissions for recurrent pneumothoraces, ultimately managed with chemical pleurodesis. Discussion Sarcoidosis likely results from a multifactorial immune response to persistent inhaled antigens shaped by environmental and host factors. Globally, nearly three billion people rely on coal and biomass fuels for cooking and heating, creating substantial exposure to particulate matter and organic antigens. Chronic biomass smoke inhalation has been linked to COPD, bronchial anthracofibrosis, and interstitial pneumonitis, but sarcoid-like granulomatous reactions from biomass exposure remain underrecognized. This case highlights the potential for chronic biomass smoke inhalation to induce granulomatous inflammation and fibrotic lung disease resembling sarcoidosis. Recognition of environmental exposures such as biomass fuel burning is essential in evaluating patients with granulomatous lung disease, particularly those from regions where indoor biomass use is common. Early identification and targeted therapy may mitigate progression to advanced fibrosis and cardiopulmonary complications. This abstract is funded by: None
Fernandez et al. (Fri,) studied this question.