An 85-year-old man was referred to our hospital for further evaluation of exertional dyspnea for 6 months with a modified Medical Research Council (mMRC) dyspnea scale of grade 1. Four years prior, he had complained of a few weeks' history of coughing, pharyngeal pain, and wheezing, which were treated at another hospital with short-term intravenous corticosteroids and oral antibiotics, based on a diagnosis of asthma exacerbation due to upper respiratory tract infection. He had never smoked; but was occupationally exposed to silica dust from the fourth to the seventh decades of his life when he worked at a motorcycle manufacturing company, where he handled sand mold casting without the use of any respiratory protection. All members of his family were never-smokers and while some colleagues at the same factory were smokers, they had scarcely smoked in the factory. His medical history included hypertension and diabetes.
A physical examination was unremarkable, and the breath sounds were normal for both lungs. The laboratory findings were not contributory. The serum immunoglobulin E level was 6 IU/mL; radioallergosorbent tests against common inhaled allergens were all negative. Serum autoantibodies, including rheumatoid factor, anti-cyclic citrullinated peptide antibody, and anti-nuclear, anti-SS-A, and SS-B antibodies, were also negative. The fractional exhaled nitric oxide concentration measured by NIOX MINO (Aerocrine, Solna, Sweden) was 15 ppb. The findings on a bronchial provocation test with acetylcholine chloride was negative. The results of a pulmonary function test were as follows: vital capacity 2.70 L (90.6% predicted), forced vital capacity (FVC) 2.69 L (90.3% predicted), forced expiratory volume in 1 second (FEV1.0) 1.16 L (62.7% predicted), FEV1.0/FVC 43.12%, maximum mid-expiratory flow rate 0.25 L/sec (10.6% predicted), residual volume per total lung capacity 43.98% (110.4% predicted), diffusion capacity of the lung for carbon monoxide (DLco) 13.67 mL/min/mmHg (85.3% predicted), and DLco divided by the alveolar volume 3.57 mL/min/mmHg (90.2% predicted). The bronchial reversibility after ultrasonic nebulization with procaterol hydrochloride was 10.3%. An arterial blood gas analysis on room air showed pH 7.406; arterial oxygen tension 87.3 mmHg; and arterial carbon dioxide tension 40.2 mmHg. On a sputum smear, numerous neutrophils without eosinophils were observed. Chest radiograph showed no abnormalities (Fig. 1A), and high resolution computed tomography (HRCT) of the chest showed thickening of the bronchial walls without emphysema (Fig. 1B and C). The macroscopic findings on fiberoptic bronchoscopy were unremarkable. A transbronchial lung biopsy (TBLB) showed fibrosis and slight pigmentation of the bronchioles (Fig. 2) with small crystals viewed by polarized light microscopy, suggestive of silica exposure.
Non-smoking COPD caused by silica dust was diagnosed, and he was treated with olodaterol and tiotropium bromide. Eight weeks after the initiation of treatment, his exertional dyspnea improved from mMRC grade 1 to 0, and the COPD assessment test score decreased from 7 to 2. Although his airflow obstruction did not improve, his inspiratory capacity increased from 1.86 to 2.01 L on the pulmonary function test.
Computed tomography of the chest shows thickening of the bronchial wall without emphysema (B, C).