The general work procedures of a dental technician include model marking, waxing up, investing, burn-out, casting, devesting, metal trimming, and polishing. In these processes, the workers are exposed to metal dust or fumes from casting and metal trimming, and the polishing and porcelain working rooms are where a person can be exposed to such dust. The size of dust particles to which a dental technician is exposed while performing metal trimming and polishing is about 0.3-5 μm, and studies have found that the dust can cause health problems . Hong et al  who analyzed the main constituents of the exposure in a dental technician’s work place reported that MMA is a major particle of exposure.
Exposure assessment of workplace
A dental technician’s work includes the following processes: polishing metal alloy acquired by casting with a diamond disk, stone point, or carbon steel tool; a washing phase such as ultrasound cleaning and smoothing surfaces by blasting with 5-μm aluminum oxide particles; a building process in which metal held in the proper position by porcelain is heated in a calcination furnace; a forming process that shapes metal alloy or resin to fit a patient’s dental and oral structures; and glossing and polishing ceramic and metal surfaces with diamond disks. Among them, the disking, forming, and polishing processes have a risk of exposure to metal and resin dust. For protection, the dental technician patient used a disposable medical mask during the manufacturing process, but no gloves were used. Polishing is a dry process in which a machine is driven manually. A dust collector is built into the working desk, and it pulls the dust under the desk. The melting work table has a hood-type fume collector installed.
Dental technician exposure to MMA or metal dust has been reported previously. In Korea, Hong et al. researched the chemical risk factors  for dental technicians working in the Ulsan area. In that study, the size of the dental laboratory was 6.3 workers on average, and 10 out of 14 laboratories employed fewer than 10 people. Our patient worked in a similar environment to that described by Hong et al.’s study. The patient had worked in a laboratory where 3 technicians were working, and the size of the work area was about 30-60 m2. Although this study did not perform direct measures of the level of exposure within the patient’s work place, the study of Hong et al. can provide indirect data on the nature of the working conditions for the present case. According to Hong et al., all 16 places were found to have manganese, cobalt, and chrome dusts as well as MMA. Since MMA induced hypersensitivity pneumonitis has been reported  and MMA causes pathologic condition dependent on an individual’s immune process rather than the level of MMA exposure, MMA is considered a major risk to dental technicians.
HP is an interstitial disease caused by consistent and repeated exposure to dust that incites an immune reaction to the lung interstitium and alveola. Clinically, it is divided into acute, subacute, and chronic types. In the acute phase, flu like symptoms such as cough and dyspnea develop. The subacute phase proceeds for several weeks, and it is characterized by mild fever and exertional dyspnea. In the chronic type, repeated exposure to a low quantity of causative particles provokes chronic bronchitis symptoms such as exertional dyspnea, cough, and sputum, and along with the symptoms, patient may also complain of weight loss and mild fever. In the chronic type, irreversible changes, including fibrosis of lung tissue may be evident. It is imperative to consider HP in a person whose pulmonary symptoms are suspected to be related with a workplace or environment which there is a risk of organic dust exposure. In addition, when repeated episodes of symptom relapse and recovery in a person who is exposed to antigens that are known to cause HP are present, clinical work-ups are recommended .
The etiology of the disease is still unknown, but it is currently believed to be due to a cell-mediated and humoral immune reaction that is caused by aspirated antigen. When antibody complex is formed with aspirated antigens, the macrophages are activated. In turn, interleukin (IL)-1,-2,-6, and-8, interferon (IFN)-γ, tumor necrotizing factor (TNF)-, and macrophage inflammatory protein-1α are secreted. Initially, the number of neutrophils are increased, and later T-lymphocytes and monocytes become dominant. In the early stage, the number of CD4+ lymphocytes increases, but the number of CD8+ lymphocytes increases in the later stage, lowering the CD4+/CD8+ ratio . A delayed hypersensitivity reaction is manifested by helper T1 cells including granulomas and fibrotic changes in the peribronchiolar area, and IL-12 secreted by activated macrophages is involved with differentiation from T0 to T1 cells . The known causes of HP are antigens derived from animals and plants, low molecular weight chemical substances, microorganisms such as bacteria and fungi, drugs, and metal dusts. Occupationally and environmentally, light metals including cobalt and aluminum, beryllium, and MMA are also known to incite HP.
In the acute stage, hypersensitivity pneumonitis manifests fever, myalgia, cough and dyspnea starting 4 to 12 hours after exposure. With discontinuation of the exposure, the symptoms are self-limiting within a few days. Further exposure leads to the subacute stage, and several days or weeks of exposure incites symptoms such as cough and dyspnea that subside within a few weeks to months without further exposure. The protracted acute or subacute phase may develop into the chronic stage . Then chest radiograph shows centrilobular nodules, ground glass opacity, airspace consolidation, and a mosaic pattern in the acute and subacute types, and in the chronic type, fibrosis and emphysema are the dominant findings . BAL shows lymphocytosis with a decreased CD4+/CD8+ ratio. Interstitial lymphocyte infiltration and noncaseating granuloma are characteristic findings histologically. A simple spirometer test reveals both restrictive and obstructive patterned ventilatory dysfunction, and the pulmonary diffusing capacity is lowered. A provoking test induced by aspirating causative particles is helpful to differentiate from other interstitial lung diseases, but the test must be considered cautiously as a diagnostic tool due to the risky nature of a provoking test [9, 10].
Several diagnostic criteria have been suggested. Schuyler and Cormier proposed the following symptoms to be compatible with HP: a clear exposure history or confirmation of the causative antigen from medical tests such as a blood test or BAL, a simple chest radiograph or chest computed tomography findings compatible with HP, lymphocytosis by BAL analysis, suggestive pathologic findings in a lung biopsy sample, and relapse of the disease when exposed to the causative particles again as the major diagnostic criteria, along with crackles in both lungs, decreased diffusing capacity, and dyspnea on exertion as minor diagnostic criteria. If a person fits 4 major criteria and 2 minor criteria, HP is diagnosed . In this case, the patient had symptoms of HP. The patient had a definite exposure history while working as a dental technician for 10 years. Both lungs showed a diffuse ground glass pattern on chest CT, and lymphocytosis was observed from the BAL fluid analysis. Finally, interstitial lymphocyte infiltration and poorly-marginated noncaseating granuloma within the lung parenchyma was present, satisfying 5 of the major diagnostic criteria suggested by Schuyler and Cormier. The patient also complained of dyspnea on exertion, satisfying 1 minor criterion. This case had an increased CD4+/CD8+ ratio, and this finding is not compatible with the typical findings of HP, in which the ratio is lowered. However, in some cases, the CD4+/CD8+ ratio that can help differentiate between HP and sarcoidosis has been found to be as high in HP as in sarcoidosis. Thus, some reports have noted that the ratio cannot be a characteristic finding in HP . Since the patient’s symptoms had improved after avoiding exposure and angiotensin-converting enzyme and rheumatoid factor were found to be normal, it is reasonable to make a diagnosis of HP in this case. Lastly, this case had been confirmed by pathology, and giant cells are considered to be findings suggesting giant cell interstitial pneumonia (GIP). Generally, confirming the presence of giant cells on histologic testing is an important pathognomonic finding in making a diagnosis of GIP when a person’s clinical manifestation is suspicious. If giant cells are identified on histologic testing, they present as many giant cell infiltrations, mostly in the interstitium and alveolar lumen. Giant cells are usually found in pulmonary tuberculosis, foreign bodies, and HP. If a low number of giant cells are present, this may suggest non-specific findings, and careful interpretation is required with counting in clinical progression and laboratory findings in making a diagnosis of a lung disease. However, in our case, the infiltration was found diffusely but minimally in both lungs, and interstitial lymphocyte infiltration and noncaseating granuloma that had an ill-defined demarcation with the lung parenchyma were other histological findings. Considering these findings, our case was more compatible with the findings of HP or dental technician’s pneumonitis in pathologic terms than with the findings of GIP. MMA, which is the presumptive particle causing the patient’s clinical manifestation, has been reported to incite immune related lung diseases such as occupational asthma and HP , and in an animal study, MMA was demonstrated to provoke subacute pneumonitis . The etiology of HP induced by MMA is believed to be a humoral and cell-mediated immune reaction resulting in antibody complex formation. In turn, the formation activates macrophages that secrete various cytokines, creating fibrosis and granuloma, and as in our case, macrophages are characteristically observed in BAL fluid .
The treatment for HP is early diagnosis and avoidance of the antigen. When clinical symptoms are severe, systemic steroid hormone can be administered . Prednisolone was given to the patient in our case, and the treatment improved the dyspnea and chest CT findings. She quit her job 3 months after being diagnosed with HP, and the prednisolone was tapered and eventually discontinued at 5 months after initiating the administration. Her symptoms improved significantly after she began avoiding exposure, and she no longer complained of any symptoms in her daily activities.
Assessment of work-relatedness
Because HP has nonspecific clinical symptoms, a differential diagnosis with other diseases that cause fibrotic changes in the lung parenchyma are necessary. Therefore, to make a diagnosis of HP properly by differentiating from other lung diseases such as pulmonary tuberculosis, histoplasmosis, rheumatoid nodules, sarcoidosis, pneumoconiosis, and giant cell interstitial pneumonia, evidence of an exposure history and radiologic and laboratory tests are required. GIP, in particular, which is characterized by multinucleated giant cells, has clinical and laboratory findings similar to HP, requiring careful interpretation . In our case, the patient had undergone transbronchial lung biopsy, and multinucleated giant cells were present in the sample. However, the giant cell presence was minimal but diffusely spread over the tissue, and in addition lymphocyte infiltration and noncaseating granuloma that did not have a clear border with the lung parenchyma were also observed. With these findings, the diagnosis was made as subacute HP or dental technician’s pneumoconiosis in pathologic terms. To find an association of the occupation with the patient’s condition, it is important to exclude other causes or exposures that may have derived from patient’s growth, residential environment, and hobbies. The patient had resided and been raised in an urban apartment, and she did not possess any hobby or other jobs that would suggest exposure to dust. Considering that her father worked as a white collar professional in a printing business and her mother was a homemaker, any secondary exposure from a family member could also be excluded. The patient’s symptomatic clinical progression had improved after avoiding workplace exposure. Therefore, because the patient has no other causes besides her occupational exposure and her condition had improved without further exposure to dust, we were able to determine with a high degree of certainty that her pneumonitis was associated with her occupation.
In light often clinical investigation and literature review, her condition was well-suited for making a diagnosis of HP. While evaluating her work environment, suspected MMA and light metal dusts were found. While working, it was confirmed that she was not provided with proper protection equipment, and her condition improved after quitting her job. She did not have any familial history or other jobs or hobbies that may have exposed her to the condition. These findings suggest strong work-relatedness.
This case is important that it is the second case of HP in a dental technician diagnosed in Korea. In Korea, the first case of HP in a dental technician was recognized as a occupational disease in 2005. The study has limitations in that a direct evaluation of the level of dust exposure within the workplace was not performed, and the follow-up time could have been longer. However, despite these limitations, the investigation process made in this case was valuable in that it may assist in making a diagnosis of lung parenchymal diseases in other patients and in evaluating the work-relatedness of diseases in dental technicians and those working in similar fields.
In addition, it should be noted that, the HP of a dental technician is probably work-related if the clinical signs and symptoms were subside when exposure to the workplace ends. In future, when a nonspecific case with suspicion of work-related HP is encountered, much effort will be necessary to make long-term observations of changes in the patient’s clinical condition and to perform the required examinations, including invasive ones.
Written informed consent was obtained form the patient for the publication of this report and any accompanying images.