doi: 10.2169/internalmedicine.8860-17Intern Med 56: 3323-3326, 2017
http://internmed.jp【 CASE REPORT 】

Dental Technicians’ Pneumoconiosis
Masaki Okamoto 1, Masaki Tominaga 1, Shigeki Shimizu 2, Chiyo Yano 1, Ken Masuda 1,
Masayuki Nakamura 1, Yoshiaki Zaizen 1, Takashi Nouno 1, Satoshi Sakamoto 1,Mitsuru Yokoyama 3, Tomotaka Kawayama 1 and Tomoaki Hoshino 1

Abstract:
A 40-year-old female dental technician visited our hospital for the investigation of a chest X-ray abnormality. Chest computed tomography demonstrated centrilobular nodules and lung volume reduction, and her serum KL-6 level was elevated. A histological analysis of the specimens obtained on a surgical lung biopsy
showed peribronchiolar fibrosis with pigmented macrophages and cholesterol clefts. An energy-dispersive Xray analysis showed that these lung tissues contained some metals, including indium. The serum indium level
was also elevated. We diagnosed this patient with pneumoconiosis caused by exposure to sandblasting certain
dental metals. This is the first reported case of pneumoconiosis in a dental technician associated with exposure to indium.
Key words: dental technician, pneumoconiosis, indium(Intern Med 56: 3323-3326, 2017)(DOI: 10.2169/internalmedicine.8860-17)

Introduction
Pneumoconiosis is a fibrotic pulmonary disease caused by
the accumulation of inhaled particles in the lungs. It is an
important occupational disease because it leads to chronic
respiratory failure with a high risk of complicating tuberculosis and lung cancer (1). Dental technicians are exposed tovarious airborne particles because their work includes thesandblasting of dental metals. Therefore, their working conditions carry a risk of pneumoconiosis (2-14). Indium is arare element included in indium-tin oxide (ITO), a material
in flat-panel displays or plasma display panels for televisionscreens, and has been reported as a risk factor for occupational lung disease (15-19). We herein report for the firsttime a case of pneumoconiosis in a dental technician associated with exposure to dental metals including indium.

Case Report
A 40-year-old woman visited our hospital in October

2015 because of an abnormality on a chest X-ray film taken
during a health checkup. She had no symptoms, such as
coughing or shortness of breath. She had never smoked andhad no history of respiratory disease. She had worked as adental technician since 20 years of age and had been engaged in the sandblasting of dental metals for 20 years. She
had no occupational history of exposure except as a dentaltechnician.
Her vital signs on admission were as follows: respiratory
rate, 20/min; heart rate, 84/min; blood pressure, 91/50
mmHg; and body temperature, 36.3°C. A physical examination and blood hematology gave normal results. She had nofine crackles or clubbed fingers. Hematology and laboratory
examinations revealed elevation of the erythrocyte sedimentation rate (ESR 40 mm/h) and the serum levels of lactate
dehydrogenase (LDH 302 IU/L) and KL-6 (1,797 IU/mL) as
biomarkers of interstitial lung disease (ILD). Diagnostic
biomarkers of connective tissue diseases, such as rheumatoid
factor and antinuclear antibody, were negative. An arterial
blood gas analysis indicated no abnormalities, such as hypoxemia or hypercapnia (PaO2 95.4 Torr, PaCO2 38.4 Torr).

１Division of Respirology, Neurology and Rheumatology, Department of Internal Medicine, Kurume University School of Medicine, Japan, ２ Department of Pathology, Kindai University Faculty of Medicine, Japan and ３ Shared-Use Research Center, University of Occupational and Environmental Health, Japan
Received: January 13, 2017; Accepted: March 27, 2017; Advance Publication by J-STAGE: October 11, 2017
Correspondence to Dr. Masaki Okamoto, okamoto_masaki@med.kurume-u.ac.jp3323

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DOI: 10.2169/internalmedicine.8860-17

A

BFigure 1. Chest X-ray film (A) showing parenchymal linear lesions and lung volume reduction predominantly in both upper lobes. Chest high-resolution computed tomography images (B) showing
subpleural pulmonary opacity (black arrow) in the right upper lobe and centrilobular nodules (whitearrow), parenchymal linear lesions, and ground-glass attenuation predominantly in both upper lobes.

Chest X-ray and high-resolution computed tomography(HRCT) demonstrated parenchymal linear lesions, centrilobular nodules, subpleural fibrosis, and lung volume reduction, predominantly in both upper lobes (Fig. 1). Pulmonary
function tests demonstrated restrictive ventilatory impairment(forced vital capacity 67.9% of that predicted, total lung capacity 68.0% of that predicted, forced expiratory volume
1.0% 86.7%, residual volume 128% of that predicted). A
six-minute walking test yielded a distance of 519.2 m and aminimum SpO2 of 95%. No bacterial or fast-acid bacillus
bodies or atypical cells were found in bronchoalveolar lavage fluid. Transbronchial lung biopsy specimens showed
only non-specific inflammation of the alveolar septa. The
differential diagnosis included pneumoconiosis, chronic hypersensitivity pneumonia, and pleuroparenchymal fibroelastosis (PPFE).
We performed a surgical lung biopsy using video-assisted
thoracoscopy to establish a diagnosis. A histological examination revealed patchy and peribronchiolar fibrosis and fibroelastosis with pigmented macrophages and marked foreign body granuloma with cholesterol clefts in both the alveolar spaces and interstitium in specimens from the rightS2 and S6 segments (Fig. 2A, B). The peribronchiolar distribution of fibroelastosis was inconsistent with the histologicalpattern of PPFE. These findings were consistent with pneumoconiosis, particularly indium-associated lung disease. A
microanalysis using an energy-dispersive X-ray analytical
spectrometer (TM3000+Quantax70; HITACHI, Tokyo, Japan) showed that the affected lung tissues contained metallic
particles, such as aluminum (Al), silver (Ag), titanium (Ti),cobalt (Co), nickel (Ni), chromium (Cr), and indium (In)(Fig. 2C). An inductively coupled plasma mass spectrometry
analysis showed a high serum indium level at 34 μg/L (cutoff level 0.1 μg/L). Therefore, we diagnosed this patient as
having dental technicians’ pneumoconiosis caused by exposure to dental metals. We classified the case as 1/2 of thePR classification of pneumoconiosis. We advised her to use
a protective face mask to avoid regular dust exposure at her

job and requested that the person responsible in her workplace improve the environment of the dental laboratory. The
patient’s disease activity is now being monitored by periodic
examinations in our hospital, and she is currently stable.

Discussion
It has been reported that the prevalence of pneumoconiosis among dental technicians is 4.5-23.6% after a mean exposure duration of 12.8-28.4 years (2-14). Ergün et al. suggested that exposure to sandblasting is a major risk factor
that carries a 77-fold-increased risk of pneumoconiosis (2).
Patients with pneumoconiosis have micronodular and reticular lesions predominantly in both upper lobes of the lungand restrictive and/or obstructive pulmonary function impairment (2). Previous studies have shown that dental technicians have more respiratory symptoms and lower pulmonary
function than controls in other lines of work (3, 6-9). Employment duration is positively correlated with the extent ofradiological abnormalities and negatively correlated with thepulmonary function (3, 10-12). In addition, Dogan et al. reported that the prevalence of pneumoconiosis among 36
dental technicians increased from 13.8% to 47% and that theradiologic findings and pulmonary function worsened significantly during 7 years of continuous work in the sameplace (13). These results suggest that exposure to dental
metals is an obvious risk factor for the development ofpneumoconiosis in dental technicians. Preventive measuresagainst exposure to dental metals may be insufficient. Choudat et al. investigated 105 self-employed dental technicians
living in Paris and found that they often worked alone(43.7%) or in small laboratories without adequate dust control (3). Seldén et al. suggested that local exhaust ventilation
might reduce the risk of exposure to dental metals (14).
Various measures are therefore needed to protect the healthand hygiene of dental technicians.
Previous reports have suggested that the substances thatcause pneumoconiosis include silica, nickel-chromium, as-3324

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ABC
Figure 2. Histological findings in the specimen obtained by a surgical lung biopsy. Hematoxylin
and Eosin staining showing patchy peribronchiolar fibrosis and fibroelastosis with pigmented macrophages and marked foreign body granuloma with cholesterol clefts in both the alveolar spaces andinterstitium (A, B: right S6). A microanalysis using an energy-dispersive X-ray analytical spectrometer revealed peaks for several metallic elements used in dental devices (C).

bestos, beryllium, cobalt, and other components of dentalmetals (2). We described the first case of dental technicians’
pneumoconiosis caused by exposure to indium in the present
case report. Several cases of lung disease have been reported
in plant workers exposed to indium (15-19). Cummings etal. reported 10 clinical cases of lung disease in indium
workers (15). Histologically, indium lung disease is characterized by peribronchiolar fibrosis with the accumulation ofmacrophages and numerous cholesterol clefts (16). The present case also showed histological findings similar to those
associated with indium lung disease. Some cases of pneumoconiosis might have been diagnosed as indium lung disease. Nogami et al. reported that the serum level of KL-6 asa biomarker of ILD was elevated in patients with indium
lung disease and was correlated with the serum indium
level (19). The histological findings in the lung and elevation of the KL-6 serum level in the present case were compatible with indium lung disease. The clinical course of indium lung disease is progressive (15, 17). Cummings et al.
reported that 2 of their 10 cases were fatal (15). The present
case report is important because it draws attention to thepossible development of progressive indium lung disease indental technicians.
Recent improvements in dental medical technology andincreases in the demand for dental materials will make it
more important to adopt protective measures against dust
exposure in dental technicians.
The authors state that they have no Conflict of Interest (COI).

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