Characterization and toxicity evaluation of air-borne particles released by grinding from two dental resin composites in vitro.

OBJECTIVE: The project aims to evaluate whether inhalation of particles released upon grinding of dental composites may pose a health hazard to dentists. The main objective of the study was to characterize the dust from polymer-based dental composites ground with different grain sized burs and investigate particle uptake and the potential cytotoxic effects in human bronchial cells. METHODS: Polymerized blocks of two dental composites, Filtek™ Z250 and Filtek™ Z500 from 3M™ ESPE, were ground with super coarse (black) and fine (red) burs inside a glass chamber. Ultrafine airborne dust concentration and particle size distribution was measured real-time during grinding with a scanning mobility particle sizer (SMPS). Filter-collected airborne particles were characterized with dynamic light scattering (DLS) and scanning electron microscopy (SEM). Human bronchial epithelial cells (HBEC-3KT) were exposed to the dusts in dose-effect experiments. Toxicity was measured with lactate dehydrogenase (LDH) assay and cell counting kit-8 (CCK8). Cellular uptake was observed with transmission electron microscopy (TEM). RESULTS: Airborne ultrafine particles showed that most particles were in the size range 15-35 nm (SMPS). SEM analysis proved that more than 80% of the particles have a minimum Feret diameter less than 1 µm. In solution (DLS), the particles have larger diameters and tend to agglomerate. Cell toxicity (LDH, CCK8) is shown after 48 h and 72 h exposure times and at the highest doses. TEM showed presence of the particles within the cell cytoplasm. SIGNIFICANCE: Prolonged and frequent exposure through inhalation may have negative health implications for dentists.

Hyphae fragments from A. fumigatus sensitize lung cells to silica particles (Min-U-Sil): Increased release of IL-1ß.

Exposure to particulate matter (PM), such as mineral particles and biological particles/components may be linked to aggravation of respiratory diseases, including asthma. Here we report that exposure to Aspergillus fumigatus hyphae fragments (AFH) and lipopolysaccharide (LPS) induced both mRNA synthesis and release of pro-inflammatory interleukin-1 beta (IL-1ß) in both human THP-1 monocytes (THP-1 Mo) and phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 monocytes (THP-1 macrophages; THP-1 Ma); while Min-U-Sil alone enhanced the release of IL-1ß only in THP-1 Ma. Co-exposure to LPS or AFH with Min-U-Sil caused a synergistic release of IL-1ß when compared to single exposures. In contrast, Min-U-Sil did not markedly change LPS- and AFH-induced release of tumor necrosis factor alpha (TNF-α). The combined exposures did not increase the LPS- and AFH-induced expression of IL-1ß mRNA. Notably, the AFH- and LPS-induced IL-1ß responses with and without co-exposure to Min-U-Sil in THP-1 Mo were found to be caspase-dependent as shown by inhibition with zYVAD-fmk. Furthermore, co-exposure with AFH and Min-U-Sil resulted in similar synergistic releases of IL-1ß in primary human airway macrophages (AM; sputum), peripheral blood monocyte-derived macrophages (MDM) and in the human bronchial epithelial cell line (BEAS-2B). In conclusion, AFH induce both the synthesis and release of IL-1ß. However, Min-U-Sil further enhanced the cleavage of the induced pro-IL-1ß.