RESTRICTIVE HUT LUNG: A CASE OF DOMESTICALLY-ACQUIRED PNEUMOCONIOSIS WITH A SEVERE RESTRICTIVE PATTERN

Abstract

SESSION TITLE: Medical Student/Resident Occupational and Environmental Lung Disease SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Domestically acquired particulate lung disease (DAPLD) or “hut lung” is a mixed-dust pneumoconiosis that develops secondary to the inhalation of biomass fuels in poorly ventilated domestic settings (1). DAPLD has largely been considered to be an obstructive lung disease, with only a minority of cases reporting mild restrictive or mixed patterns of disease (1). To our knowledge, this is the first case report of DAPLD with a severe restrictive pattern. CASE PRESENTATION: A 76 year old Hispanic woman presented with worsening shortness of breath for one year, associated with reduced exercise tolerance, nonproductive cough, chest tightness, and wheezing. She spends majority of the year in Honduras, but travels to the United States for the summer months. She denied smoking tobacco and occupational exposures, but admitted to using a wood burning stove for cooking while living in Honduras for many years. CXR was notable for bilateral patchy infiltrates. HRCT showed large patchy and confluent areas of ground glass attenuation in association with linear and reticular opacities, and peripheral honeycombing with cystic changes. Small calcified bilateral hilar lymph nodes were also observed. Quantiferon testing was positive, but serial cultures were negative for tuberculosis. PFTs showed a restrictive pattern: FEV1 82%, FVC 59%, FEV1/FVC 95%, TLC 46%, DLCO 7%. Bronchoscopy showed multiple flat anthracotic plaques; transbronchial biopsy of these lesions demonstrated focal chronic inflammation. BAL cytology and cultures were unremarkable. DISCUSSION: Although the prevalence of DAPLD is unknown, inhalation of particulate residue of biomass fuels used for domestic energy is common in several parts of the world (2). Cooking with biomass fuels may be associated with fine particle carbon dispersion (2). Deposition of biomass fine particles along alveolar surfaces and macrophage activation initiates an inflammatory response (2). Discourse on biomass inhalation and tobacco smoking has focused on the development of COPD, however both of these exposures may also result in ILD (3). Type 2 alveolar epithelial stem cells, which may function as both type I and type II alveolar cells, have been proposed to play a central role in predisposing patients with tobacco and biomass exposure, to both COPD and ILD phenotypes (2,3). Tobacco and biomass have been proposed to induce cellular senescence, which allows for genetic remodeling and profibrotic cellular changes (2,3). Predisposition of these stem cells to senescence would make certain patients susceptible to COPD or ILD based on the chosen behavior of the stem cell (3). CONCLUSIONS: While the body of research on the hazards of exposure to biomass continues to grow, the restrictive phenotype of DAPLD remains a rare condition that requires further research. Reference #1: Dulku, G, Gupta, N, Perera, R, et al. 2017. Hut Lung Disease: A Radiological and Pathological Correlation. J Med Imaging Case Rep 1(1): 1-4. Reference #2: Kunal S, Pilaniya V, Shah A. 2016. Bronchial Anthracofibrosis with Interstitial Lung Disease: An Association Yet to be Highlighted. BMJ Case Rep bcr2015213940. Reference #3: Kumar, A, Cherian, SV, Vassallo, R, et al. 2018. Current Concepts in Pathogenesis, Diagnosis, and Management of Smoking-Related Interstitial Lung Diseases. Chest 154(2): 394-408. DISCLOSURES: No relevant relationships by Rose Flores, source=Web Response No relevant relationships by Johnathan Kirupakaran, source=Web Response No relevant relationships by Chioma Madu, source=Web Response No relevant relationships by Alice Yau, source=Web Response