CHRONIC EOSINOPHILIC PNEUMONIA IN AN AIR-BRUSH PAINTER WITH POOR RESPONSE TO SYSTEMIC STEROIDS

SESSION TITLE: Medical Student/Resident Occupational and Environmental Lung Diseases SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Air-brush paints contain low molecular weight chemicals that can cause occupational asthma, respiratory sensitization and hypersensitivity pneumonitis; however, its relationship to Chronic Eosinophilic Pneumonia (CEP) has never been reported. Hereby, we describe a case of CEP in a patient who was exposed to air-brush paints for a long time. CASE PRESENTATION: A 48-year-old male, who worked as an air-brush painter for 20 years, presented with exertional dyspnea and cough productive of clear sputum for 4 weeks. He also had pleuritic chest pain, low grade fever, chills, malaise, and 10 lbs. weight loss. He had 12 pack-year smoking history and quit 2 years ago. Chest exam revealed bilateral basilar coarse crackles. White Blood Cell (WBC) count showed mild leukocytosis with Eosinophils (E) 5%, absolute E count 500/μL, elevated CRP and negative Procalcitonin. Computed Tomography (CT) of the chest (Figure 1) showed bilateral lower lobes infiltrates and ground glass opacities. After 2 days, his WBC count jumped to 17,000 with E% 7.5 and absolute E count 1300/μL with worsening oxygen requirement. Bronchoscopy was not performed due to his high oxygen requirement. However, because of patient’s progressive symptoms and despite being at high risk, open lung biopsy was done for definitive diagnosis. Pathological examination (Figure 2) revealed CEP with organizing pneumonia pattern. He was then started on high-dose systemic steroids with gradual tapering but adequate clinical recovery was not achieved. His hospital course was also complicated by pneumothorax and trapped lung too, and he continued to have high oxygen requirement. A repeat CT of the chest (Figure 3) showed worsening of lung infiltrates and fibrosis. DISCUSSION: Our patient was exposed to air-brush paints for 20 years and presented with CEP; thus, we believe it is warranted to investigate the relationship between CEP and occupational exposures, such as air-brush painting. Generally, patients with CEP have excellent response to systemic steroids and avoidance of the hypothetical inciting factor; however, our patient had poor response to systemic steroids. We believe that his prolonged exposure to air-brush paints and the additional pathology of organizing pneumonia might have contributed to the unsatisfactory response to systemic steroids, prolonged hypoxia, and the overall worse prognosis. CONCLUSIONS: We are presenting a unique association between CEP and prolonged exposure to air-brush paints. In this case, the patient had poor response to systemic steroids too, which was likely due to prolonged occupational exposure in addition to the evolution of progressive fibrosis and organizing pneumonia. Reference #1: Plitnick LM, Loveless SE, Ladics GS, Holsapple MP, Smialowicz RJ, Woolhiser MR, et al. Cytokine mRNA profiles for isocyanates with known and unknown potential to induce respiratory sensitization. Toxicology 2005; 207: 487-99. Reference #2: Di Stefano F, Di Giampaolo L, Verna N, Di Gioacchino M. Occupational eosinophilic bronchitis in a foundry worker exposed to isocyanate and a baker exposed to flour. Thorax 2007; 62: 368-70. Reference #3: Carrington CB, Addington WW, Goff AM, Madoff IM, Marks A, Schwaber JR, et al. Chronic eosinophilic pneumonia. New Engl J Med 1969; 280: 787-98. DISCLOSURES: No relevant relationships by Ravindra Bharadwaj, source=Web Response No relevant relationships by Manish Patel, source=Web Response No relevant relationships by Nethuja salagundla, source=Admin input No relevant relationships by AHMED TAHA, source=Web Response No relevant relationships by Thien Vo, source=Web Response