Three cases of dental technician’s pneumoconiosis related to cobalt-chromium-molybdenum dust exposure: diagnosis and follow-up
Dental technician’s pneumoconiosis (DTP) is a rather recent finding in subjects exposed to the dust generated in dental laboratories producing metal-framed removable partial dentures from alloys based on cobalt, chromium, and molybdenum. This study presents details of the first three Swedish cases of DTP with some emphasis on the diagnostic procedures and the dust exposure. A follow-up of at least 5 years from diagnosis is included.
Key words: case report; dental alloys; dental technicians; dust; etiology; minerals; pneumoconiosis
Pneumoconiosis in a dental technician was reported already in 1939. The case was diagnosed as silicotuberculosis and was probably caused by a polishing powder with approximately 50% free silica.(1) Additional studies on silicosis in dental technicians followed,(2) (3) (4) (5) (6) but more recent publications on pneumoconiosis in mechanical dentistry have emphasized the influence of dust generated in working with nonprecious metals, cobalt-chromium-molybdenum (CoCrMo) alloys in particular.(7) (8) (9) (10) (11) (12) (13) This report describes the first three Swedish cases of pneumoconiosis identified in dental technicians working with these alloys and includes a follow-up of 5 years or more from diagnosis.
This 50-year-old man (the index case) had worked in various dental laboratories for 30 years and was a regular smoker of 20 cigarettes a day over this period. After 5 years as an apprentice in mechanical dentistry, he worked for 3 years at a storage house and 2 years as an excavator driver in a commercial sandpit. Returning to his profession in 1962, he worked almost exclusively with the manufacture of metal-framed removable partial dentures in CoCrMo alloys until 1985. For the last 13 years of this period, he was self-employed, often working 70 to 80 h a week. Local exhaust ventilation was never available, and even the general ventilation had been poor. Overall, he had been exposed to inorganic dust from silica (investment powders and sea sand for shot blasting), asbestos (insulating bands for investment emulsions), CoCrMo, and various components of the abrasives used for grinding and polishing. No quantitative exposure data, however, were available.
His medical history was uneventful until 1978, when he complained of fatigue and exercise-induced dyspnea. A chest radiograph was normal, but no spirometry was performed. Leaving self-employment in the autumn of 1985, he eventually became the subject of a preemployment examination in November. New radiographs showed bilateral reticulonodular infiltrates, mainly at the hilar level (Fig 1, top). Sarcoidosis was suspected, but because of radiographic progression and deterioration of lung function, further examinations were carried out in the autumn of 1986. A percutaneous lung biopsy was interpreted as showing pneumoconiosis caused by silica and iron oxide. At bronchoscopy, histologically normal bronchial mucosa was found, but representative transbronchial biopsy specimens were not obtained. Cervical me diastinoscopy showed lymph nodes containing birefringent crystals suggestive of silicosis. An open-lung biopsy was performed in April 1987.
Rounded or stellate, partly confluent, fibrotic areas, sometimes with central hyalinization, were observed. The fibrosis was sometimes subpleural, and small areas with interstitial fibrosis were also found (Fig 2). In the cellular areas, both fibroblasts and myofibroblasts were observed along with inflammatory cells and macrophages, whereas no giant cells were noted. Dust-laden macrophages were numerous in the alveoli, around respiratory bronchioli, around the small vessels accompanying the bronchioli and in the fibrotic areas. In the fibrotic scars and the alveoli, brightly birefringent particles were frequently encountered. However, no asbestos bodies were observed. In the arteries, there was concentric or patchy intimal sclerosis and sometimes recanalized thromboembolic material. Signs of hypoxic arteriopathy with media proliferation and slight muscularization of small arteries were noted.
A laser microprobe mass spectrometry analysis(14) revealed aluminum; iron, and traces of silica in background fibrous tissue, whereas various particles contained aluminum, titanium, iron, chromium, cobalt, and molybdenum. Nickel and beryllium were not found.
After chemical digestion with sodium hypochlorite(15) or low-temperature plasma ashing,(16) a wide range of mineral elements was observed by x-ray fluorescence. Besides the elements mentioned in the laser microprobe mass spectrometry analysis, manganese, gold, mercury, copper, sodium, potassium, calcium, phosphorus, silicon, magnesium, chlorine, and zinc were noted. An x-ray diffraction analysis showed that quartz, tridymite, cristobalite, silicon carbide, talc, and aluminum oxide dominated in the crystalline phases.
In a scanning electron microscopy analysis, silicon dioxide and other silicon compounds predominated, but chrysotile, amphibole asbestos, and talc fibers were also observed as well as ferruginous bodies and CoCrMo alloy particles of various morphology. Core analysis of the ferruginous bodies showed both amosite, chrysotile, amalgam, CoCrMo, and silicon carbide (Fig 3).
Lung Function and Other Investigations
Lung function examinations in December 1985 showed normal static and dynamic spirometric volumes. Single-breath CO diffusing capacity, arterial blood gas value determinations, and [N.sub.2] slope were normal, but lung compliance was reduced (2.0 L/kPa; reference value, 2.8[+ or -]0.5). Serum angiotensin-converting enzyme was slightly increased (43 [mu]mol/min/L; normal, 7 to 30). The bronchoalveolar lavage (BAL) fluid cell distribution was normal, but the macrophages were heavily dust-laden. The BAL fluid cultures for mycobacteria and fungi were negative. Immunologic investigations of serum and BAL fluid were normal.
From late 1985, this patient worked only with polymer-based prosthetic materials, but he had to retire with a disability pension in 1990. However, he continued smoking until late 1992. Gradual progression of the radiographic changes was observed (Fig 1, bottom) as well as continued deterioration of the lung function. A high-resolution computed tomogram in December 1994 showed extensive fibrotic changes with occasional emphysematous blebs in the upper parts and a compensatory emphysema in the lower parts of the lungs. After an initial, slightly restrictive pattern, the ventilatory defect became mainly obstructive. In November 1994, [FEV.sub.1] was only 0.81 (23% predicted) and the [FEV.sub.1]/FVC was 30%. Total lung capacity was in the lower normal range (6.8 L; 88% predicted) and diffusion capacity was slightly lowered (5.7 mmol/min/kPa; normal, [greater than]7.8). The [PaO.sub.2] at rest was below normal, 8.9 kPa.
In a survey of dental technicians,(17) a chest radiograph obtained in March 1988 from a 30-year-old nonsmoking man showed disseminated reticulonodular opacities in the upper halves of the lungs. A previous radiograph from 1977 was normal. Starting as an apprentice of mechanical dentistry in June 1976, he had worked in the profession for 11 years, almost exclusively producing CoCrMo applications. He spent 6 years in the same dental laboratory where patient 1 had worked in the 1960s and was exposed to a similar complex mixture of inorganic dust. However, steel or aluminum pellets had been substituted for sea sand in shot blasting. For sporadic gold castings, cristobalite-based investment powders were used.
A transbronchial biopsy specimen from the middle lobe of the right lung revealed areas of fibrosis and presence of birefringent particles. Inflammatory cells and dust-laden macrophages were found around small vessels (venules) and in the fibrotic areas. No asbestos bodies, epithelioid cell granulomas, or giant cells were observed.
In a laser microprobe mass spectrometry analysis of lung tissue, titanium was a prominent finding, but cobalt and chromium were also present. Again, beryllium was absent but no reference was made to nickel.
The amount of lung tissue was insufficient for x-ray fluorescence and x-ray diffraction analysis. By transmission and scanning electron microscopy, respectively, particles and fibers similar to those found in case 1, ie, quartz, aluminum oxide, CoCrMo alloy fragments, as well as nickel, titanium, and copper were observed. The presence of nickel and absence of gold were in contrast with the findings in case 1.
Lung Function and Other Investigations
This patient had no respiratory symptoms, and the lung function values including the diffusing capacity were within normal limits in August 1988. A Kveim test was negative. Serum angiotensin-converting enzyme was increased, 59 [mu]mol/min/L. The BAL fluid had a normal cell distribution.
This patient remained in his profession under tight dust control for another 4 years, but in 1992 he decided to leave. His lung function has been stable and a high-resolution computed tomogram of the thorax in February 1994 showed only minimal progress of the apical fibrosis in comparison with a similar investigation in 1991.
In March 1989, a chest radiograph obtained from a 44-year-old male dental technician, participating in the same survey as case 2, showed extensive nodular opacities in the apical sections of the lungs. He smoked 10 to 15 cigarettes a day since the age of 15, was an amateur sportsman, and had no history of lung disease. This patient had been working almost exclusively with dentures based on CoCrMo alloys for 28 years at one single dental laboratory. Qualitatively, his dust exposure was similar to the other two cases, and he had used sea sand for shot blasting. Local exhaust ventilation was not available at the laboratory, but for the previous 8 years he had used a simple paper face mask during grinding and polishing of the prostheses. The cobalt dust level measured in the patient’s breathing zone for 1 day considerably exceeded the Swedish occupational exposure limit value of 0.05 [mg/m.sup.3], with an observed mean dust level of 1.6 [mg/m.sup.3]. The occupational exposure limit values for chromium and respirable silica dust (0.5 and 0.1 [mg/m.sup.3], respectively) were exceeded by approximately 50% each. For administrative reasons, medical examinations were undertaken at a different hospital from the two previous cases.
The findings of a transbronchial lung biopsy were similar to case 2, but there were more pronounced rounded fibrotic areas mixed with a fairly normal lung parenchyma.
An energy-dispersive x-ray film analysis of lung tissue showed high concentrations of titanium, chromium, silicon, aluminum, and cobalt, whereas nickel and beryllium were absent.
Lung Function and Other Investigations
This man reported no respiratory symptoms, and the lung volumes were normal. However, the CO diffusing capacity was at the lower end of the normal spectrum, and during exercise testing, the [Po.sub.2] was reduced from 12.0 kPa at rest to 10.8 kPa at 200 W. The BAL fluid was rich in black pigmented alveolar macrophages, but cultures for mycobacteria were negative. Serum angiotensin-converting enzyme was slightly increased.
The patient entered a dust-free occupation, and 5 years after the initial examination, his lung disease remained spirometrically and radiographically stable.
Dental technicians are exposed to a complex mixture of dust particles defined by the type of materials involved. Sporadically, fibrotic lung disease in dental laboratories has been associated with exposure to organic dust,(18),(19) but the present concept of dental technician’s pneumoconiosis (DTP) is largely confined to the inorganic dust emitted in the production of metal-framed removable partial dentures based on CoCrMo alloys. Several formulas with small variations are available on the market. Typically, modern CoCrMo alloys contain 60 to 66% of cobalt, 25 to 32% of chromium, 4 to 6% of molybdenum, and traces of other metals like silicon and manganese.(17) Nickel is avoided due to the risk of contact hypersensitivity, whereas beryllium, previously reported to appear in a small percentage of some formulas,(7),(10) is not known to have been present in Sweden. None of our cases showed evidence of beryllium exposure, since neither beryllium metal nor granulomas were identified in the lungs.
Clinically important functional abnormalities were observed only in one of our patients. The ventilatory defect was mainly obstructive. In silicosis, restrictive as well as obstructive patterns have been described. In our index patient, tobacco smoke may have played a contributory role in the development of airway obstruction. Interaction between smoking and occupational exposure was recently reported among workers exposed to asbestos,(20) which may induce obstructive as well as restrictive pulmonary disease.
Lung fibrosis is a rather unspecific phenomenon which may have many causes and also may be host-dependent. We found rounded or stellate, sometimes confluating areas of rather dense fibrosis, sometimes with hyalinization. However, in case 1, an open-lung biopsy also showed mainly subpleural, interstitial fibrosis. In all cases, there were numerous birefringent particles and anthracosis in the fibrotic tissue as well as in dust-laden macrophages. Truly granulomatous diseases such as chronic beryllium disease and sarcoidosis could be ruled out. Thus, as the histopathologic findings were reminiscent of both simple coal worker’s pneumoconiosis (stellate lesions) and silicosis (nodular fibrosis) as well as asbestosis (subpleural interstitial fibrosis), the most appropriate designation would probably be “mixed dust pneumoconiosis.”
The morphologic findings in our study were virtually identical to those described by Morgenroth et al,(11) who reported 30 cases of DTP. They did not discuss their morphologic findings in detail but presented a rather complicated pathogenetic theory for the interaction between dust particles and interstitial macrophages. Breakdown of the macrophages was considered necessary for the development of fibrosis. Today, however, in the pathogenetic considerations concerning silicosis, it is held that the macrophages secrete a fibrogenic factor before they are eventually killed by the silica. Thus, the process is analogous to other fibrosing diseases.(21) This is probably true also for DTP as the disease seems to have some similarities with silicosis. The difference is probably more related to the relative amounts of crystalline silicates (quartz, cristobalite, tridymite) vs other silicates in the lungs. In all our cases, there were numerous birefringent particles, which favors the presence of other silicates, since crystalline silica is just weakly birefringent. It may be noted that only one of the Morgenroth et al cases had typical silicotic nodules. It is also unlikely that the CoCrMo alloy in itself should produce the lesions. For example, in “hard metal disease” caused by tungsten alloys containing small amounts of cobalt, titanium, molybdenum, and nickel, soluble cobalt is thought to be the most dangerous compound. The hallmark of “hard metal disease” is interstitial fibrosis and numerous giant cells which can be identified as multinucleate type 2 pneumocytes by electron microscopy.(22) Such lesions, however, were not experienced in our cases. Moreover, in Wistar rats exposed for up to 3 months to a finely ground dust from a CoCrMo alloy, Brune et al(23) found dust-laden macrophages within and adjacent to the bronchial wall, but no inflammatory reaction or fibrosis was observed.
Correlating the extent of pulmonary fibrosis with the components of the dust deposits our results are also in good agreement with the Morgenroth et al(11) findings. It is interesting to note that all the elements listed from their 30 lung samples could be detected in one of our patients (case 1) except for silver. Moreover, elements not found by Morgenroth et al,(11) eg, mercury-based amalgam, were observed, again illustrating the very complex nature of inorganic dust exposure in this particular type of mechanical dentistry.
The abundance of ferruginous bodies observed in the open-lung biopsy sample of case 1 is an index of exposure to fibers in general and to asbestos in particular. The relative importance of fibers in the pathogenesis of DTP, however, remains to be elucidated. Our data do not allow for a distinction between asbestos or silicon carbide fibers or other elements such as aluminum silicate, quartz, corundum, or CoCrMo as single causative agents. As previously noted, however, the production of CoCrMo-based dentures and bridges has invariably been involved in the history of DTP cases.
Poor local exhaust ventilation in dental laboratories seems to be a universal problem. Without appropriate ventilation systems, various elements of the dust generated particularly in grinding have been found to substantially exceed levels that are considered safe.(17),(24) The need for a proper dust control should be stressed.
To our knowledge, no details of the prognosis in DTP have been published so far. Our cases were followed up for a minimum of 5 years, and the outcome over this period was highly variable and probably dependent on the total amount of dust inhaled. In case 1, the patient was judged to have had a rather massive cumulative dust exposure and presented with respiratory symptoms, and there was a fairly rapid progress of the disease. By contrast, in cases 2 and 3, the patients’ conditions were detected in a health survey and were symptom-free upon initial examination, and no or only minimal deterioration was observed over the follow-up period. The more favorable prognosis in these two cases is likely to be influenced by the early diagnosis and suggests that periodic radiologic surveys might be of value to prevent overt disease. However, such investigations should be limited to dental technicians with a significant exposure to CoCrMo dust, and indiscriminate use of chest radiography in mechanical dentistry is not recommended.
In conclusion, this report presents the first three Swedish cases of DTP with some emphasis on the diagnostic procedures and the dust exposure. A follow-up period of at least 5 years from diagnosis is included.
ACKNOWLEDGMENTS:All colleagues who participated in the clinical evaluation of these cases are gratefully acknowledged.Mrs. Margaretha Sandin to produce this report.
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