A Case of Occupational Hypersensitivity Pneumonitis Associated with Trichloroethylene
A 29-year-old man was referred to our hospital because of a severe and persistent dry cough, night sweats, and a 10 kg body weight loss over the previous two months. The dry cough and night sweats persisted for two months despite treatment at local outpatient clinic, but he did not complain of exertion-related dyspnea, malaise, or fever upon admission. He was a former smoker, but had stopped smoking five years prior. Notably, he did not have a history of asthma or pulmonary disease. He was not taking any medications or herbal medicines. He had started working in a new occupation of computer repairing 3-4 months ago, and did not use personal protective devices at workplace. Upon physical examination, there were no significant findings, and his vital signs were stable. The chest examination showed clear breath sounds without rales or wheezing, and the cardiac and abdominal examinations were also unremarkable. He had no skin rash or digital clubbing and no musculoskeletal abnormalities. We explored numerous causes for chronic cough, such as upper airway cough syndrome and gastro-esophageal reflux syndrome, but there were no specific findings.\nA chest X-ray demonstrated some reticulonodular densities on both upper lobes (). The results of a pulmonary function test were within the normal range, except for mildly reduced diffusion capacity of carbon monoxide (). A chest computed tomography (CT) scan showed tiny ill-defined centrilobular nodules prominent in both upper lobes (), which is consistent with HP. Laboratory results were as follows: complete blood count, 9,500/mm3 (neutrophil 71.6%, lymphocyte 22.6%, eosinophil 0.4%); hemoglobin, 14.6 g/dL; platelet count, 286,000/mm3; aspartate aminotransferase/alanine aminotransferase, 13/15 IU/L; total bilirubin, 0.7 mg/dL; total cholesterol, 210 mg/dL; total protein, 7.6 g/dL; blood urea nitrogen, 13.1 mg/dL; and a creatinine of 0.8 mg/dL on biochemistry test. Serum electrolytes were within the normal limits. C-Reactive protein was 0.152 mg/dL (normal range, 0-0.8 mg/dL), and the erythrocyte sedimentation rate was 9 mm/hr (normal range, 0-15 mm/hr). Urinalysis did not reveal proteinuria or glucosuria, but did show microscopic hematuria and pyuria. Serum total IgE level was slightly elevated at 125 kU/L (normal range, <100 kU/L). The panels for autoimmune markers such as antinuclear antibody, rheumatoid factor, anti-cyclic citrullinated peptide antibody, cytoplasmic anti-neutrophil cytoplasmic antibody, perinuclear anti-neutrophil cytoplasmic antibody, anti-Scl 70, anti-SS-A/Ro, and anti-SS-B/La were all within the normal limits.\nWe performed bronchoalveolar lavage (BAL) and transbronchial biopsy (TBB) in the posterior segment of the right upper lobe and in the anterior-medial segment of the right lower lobe.\nBAL revealed the presence of lymphocytes (80%), of which the ratio of CD4 and CD8 was 41.8%:50.6%. TBB showed no pathologic findings.\nAfter gathering details about his occupation, we discovered that his main role in repairing computers was to use lead welding to install capacitors on computer chip boards, and to wipe down the chip boards with TCE. His duties were performed without personal protective equipment or a proper ventilation system in the workplace. Unfortunately, we could not test his serum or urine TCE level, but his lead level in serum was 1.67 µg/L (normal range, <20 µg/L) and in urine was 6.24 µg/L (normal range, <80 µg/L), which were both within the normal range.\nWith this information, we strongly suspected that the HP was related to TCE exposure. We recommended him to change the occupation, but he could not find alternative occupation due to economic status. We started treatment with 30 mg oral prednisolone daily, and after oral prednisolone treatment, the dry cough was slightly improved, but it was not entirely resolved. For a more accurate diagnosis, he underwent surgical lung biopsy via video-associated thoracoscopy (VATS). Pathologic findings were present, which consisted of multifocal, patchy, fibroblastic proliferations, chronic inflammatory cell infiltration around the respiratory bronchiole, and associated foamy histiocytic aggregation (). With these biopsy results under the consideration of both clinical presentation and radiological findings, we reached a final diagnosis of subacute HP. After receiving the diagnosis, he returned to work, but revisited the outpatient clinic due to worsening, severe cough and anterior chest pain. Chest CT was performed and showed pneumomediastinum and slightly aggravated HP. He was exposed to TCE repeatedly after discharge from the hospital, and we think the pneumomediastinum may have been developed by aggravation of symptoms including severe cough. He was treated with high concentration oxygen and steroid pulse therapy (methylprednisolone 62.5 mg bid I.V.), but despite this, recurrent pneumothorax developed. He underwent wedge resection for two subpleural bullae at the right apex, and he underwent a thoracoscopic pleurectomy to treat the recurrent pneumothorax. After the operation, the recurrent pneumothorax resolved, but his chronic cough still remained after the steroid treatment. We recommended again strongly to change occupation, and after entering a new department, we tapered down the oral prednisolone slowly until discontinuation. After changing occupation and finishing the steroid regimen, the symptoms improved and the CT findings were almost completely resolved (, ).