• dental technician;
  • hypersensitivity pneumonitis;
  • methyl methacrylate

We report two cases of dental technicians with a diagnosis of hypersensitivity pneumonitis because of inhalation of methyl methacrylate (MMA), occurring within the first weeks of exposure to MMA.

When polishing and grinding prosthesis, dental technicians are exposed to mineral dusts and chemicals. Pneumoconiosis, asthma and hypersensitivity pneumonitis (HP) have been described, linked to silica, silicon carbide, asbestos or metals (1). Methyl methacrylate (MMA) is a monomer, commonly used in dental clinics. Previously, MMA has been shown responsible for occupational asthma, rhinoconjunctivitis, contact dermatitis or stomatitis (2, 3). We report two cases of HP induced by an exposure to MMA in students working in a dental laboratory.

Case 1. A 24-year-old female, with no medical history, was admitted for progressive severe dyspnoea and cough for 3 weeks. She had been exposed to MMA during her dental technician training in the laboratory, which had started 6 months ago. Physical examination revealed diffuse bilateral crackles. Biological results showed hypoxemia (55 mmHg). Pulmonary function tests (PFT) revealed a major diffusion alteration (45% of predicted value). Computed tomography (CT) showed a ground glass pattern (Fig. 1). An occupational HP to MMA was suspected. The patient improved in a few days under systemic corticosteroids treatment. One month later, 3 days after her return in the laboratory, she was hospitalized again for a severe dyspnoea, which reappeared the first day of re-exposure. CT-scan showed ground glass pattern again. Bronchoalveolar lavage (BAL) found a cell count of 570 000 cells/ml (10% macrophages, 60% lymphocytes, 25% neutrophils). Hypoxemia was 58 mmHg. PFT found a forced vital capacity (FVC) of 2.0l (50%) and a forced expiratory volume in 1 s (FEV1) of 0.85l (24%). Again, the patient rapidly recovered after a short oral corticosteroid therapy, and decided to definitely quit her job.


Figure 1. Chest HRCT scan obtained in a 24-year-old female presenting with progressive worsening of dyspnoea (case 1): at the level of the upper lobes: presence of ground glass opacities diffusely distributed throughout both lungs (A); at the level of the lower lobes: note the concurrent presence of ground glass opacities in the anterior parts of the lungs and areas of airspace consolidation in the right and left lower lobes, sparing a few secondary pulmonary lobules (B) (arrows).

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Case 2. A 20-year-old female was hospitalised for acute respiratory distress. She trained as dental technician for a few weeks. Physical examination revealed major dyspnoea associated with cough, and diffuse bilateral crackles. Blood analysis indicated hypoxemia (65 mmHg). PFT revealed a restrictive pattern (total lung capacity at 67% of predicted value) and pulmonary diffusion alteration. Chest X-ray showed diffuse and bilateral condensations associated with ground-glass attenuation zones. Occupational HP to MMA was suspected. A favourable outcome was slowly obtained under oral corticosteroid treatment and occupational eviction. Two months later, she was exposed, under medical care, to aerolized particles of MMA in a glass cage to confirm the diagnosis. Moderate dyspnoea was observed. BAL and PFT performed after the provocation test showed abnormalities compared with normal values obtained just before the test: increase of lymphocytes, 30% of total cell count, and decrease of carbon monoxide transfer coefficient (TLCO) (−20%).

We described two cases of HP related to MMA exposure occurring in dental technician students, and confirmed after re-exposure. Dental technicians are exposed to many mineral particles or acrylic dusts potentially involved in pneumoconiosis (asbestos, silica, chromium, etc.) (4), asthma (nickel, palladium, cobalt, acrylic resin) (1, 2) and/or HP (cobalt, beryllium) (2, 4), chronic obstructive pulmonary disease (COPD), lung cancer and fibrosis (5). The diagnosis of HP deserves to be considered in so far as exposure to MMA was responsible for clinical symptoms and resulted in biological, chest X-ray and PFT abnormalities consistent with HP (6). Differential diagnosis (infection…) were first eliminated. Duration of exposure allowed to exclude pneumoconiosis to mineral or metal particles. The exposure to the causative antigen (i.e. MMA) may result in acute, subacute, and chronic forms of HP. An acute episode usually follows a previous sensitization, as illustrated in case 1, and the intensity of the reaction (alveolitis) is related to the amount of inhaled antigen and the duration of exposure (7). The provocation tests with MMA alone reproduced the characteristic features of HP, suggesting the diagnosis of HP by inhalation of MMA rather than by other mineral particles also used in the laboratory.

MMA is an acrylic resin used for its resistance and lightness. Resins are reconstituted by mixture of powder (polymeric form of MMA) and liquid (monomeric form of MMA) for the preparation of prosthesis. Inhalation of the powder, or of the vapour produced by the volatile monomeric form during mixing is the first situation potentially dangerous for dental technicians. The second situation is linked to the environmental liberation of the polymeric form when polishing the solid plastic. Barrett (5) described the first case of interstitial lung disease related to an exposure to aerolized acrylic polymer of methacrylate in a dental student.

Even if this case was described as a pneumoconiosis, it showed usual characteristics of HP, and as in our two patients, clinical symptoms appeared within the first year of exposition to MMA during dental training. Confirming Barrett's case (5), the present two cases showed that MMA is potentially responsible for hypersensitivity pneumonitis. These data underlined the need for dental staff exposed to this substance to avoid direct contact with MMA, and to profit by adequate technical prevention measures, such as masks and local exhaust ventilation systems (8).


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